The DOI matches its Crossref record; 364 of the 366 references it cites were found in a registry or an index; 73 of the 334 sources its claims cite were checked for support.
Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair
Open accessAbstract
DNA is one of the prime molecules, and its stability is of utmost importance for proper functioning and existence of all living systems. Genotoxic chemicals and radiations exert adverse effects on genome stability. Ultraviolet radiation (UVR) (mainly UV‐B: 280–315 nm) is one of the powerful agents that can alter the normal state of life by inducing a variety of mutagenic and cytotoxic DNA lesions such as cyclobutane‐pyrimidine dimers (CPDs), 6‐4 photoproducts (6‐4PPs), and their Dewar valence isomers as well as DNA strand breaks by interfering the genome integrity. To counteract these lesions, organisms have developed a number of highly conserved repair mechanisms such as photoreactivation, base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). Additionally, double‐strand break repair (by homologous recombination and nonhomologous end joining), SOS response, cell‐cycle checkpoints, and programmed cell death (apoptosis) are also operative in various organisms with the expense of specific gene products. This review deals with UV‐induced alterations in DNA and its maintenance by various repair mechanisms.
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Claims the paper makes
118 No full text of the sources · 37 Partly supported · 28 No basis given · 16 Supported · 12 Sources not found · 10 Not checked yet · 8 Supported so far · 5 Own interpretation · 2 Couldn’t confirm · 1 Not supported · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“Bending of DNA towards the minor groove reduces CPDs formation [52].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
What the sources say
- Supportedcites [52] source
The Introduction says pyrimidine-dimer formation is more rapid when DNA bends toward the major groove. The Results and Discussion report periodic peaks near major-groove bends, supporting the converse comparison for minor-groove bending. The paper also states that the detected photoproduct pattern is dominated by cyclobutane pyrimidine dimers (CPDs). (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“It was revealed that the presence of trans-syn CPD causes distortion to a great extent than the cis-syn product by means of a kink or dislocation at the 5′-side of the dimer in double-stranded DNA [77].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 5. Differential Effects of CPDs and 6-4PPs on DNA Conformation
What the sources say
- Could not verifycites [77] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports little overall distortion and only minimal kinks in the cis-syn thymine-dimer models. Our copy does not address trans-syn CPDs or compare their distortion with cis-syn CPDs; searches for trans-syn and a 5′-side kink or dislocation found no passage establishing the claim. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Moreover, photoreactivity of adjoining adenine bases in DNA is strongly suppressed by the complementary base pairing [50, 72].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 4. UV-Induced Purine Photoproducts
What the sources say
- Not matchedcites [50]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Supportedcites [72] source
The Mechanistic Studies section reports less than 1% adenine photoproduct when poly(dA) was paired with poly(U) and infers that A–T pairing in DNA would likewise quench adenine photochemistry. The Discussion explicitly attributes the absence of adenine photoproducts in native DNA to hydrogen bonding between adenine and thymine. (LLM, conf=0.88)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“NMR and X-ray diffraction studies of the ultraviolet photoproduct, cis-syn CPD, with the S-cyanoethyl phosphotriester have revealed that the two pyrimidine bases are rotated by −29° base twist, contrasting to the right-handed 36° value observed in B-form DNA [78, 79].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 5. Differential Effects of CPDs and 6-4PPs on DNA Conformation
What the sources say
- Partly supportedcites [78] sourceExperimental — accuracy not yet measured
The Geometry of the Cyclobutane Ring section describes an NMR study of the cis-syn d(TpT) photoproduct, but says its data cannot independently assign the intact molecule’s ring configuration. The Sugar-Base Torsion Angles section reports reorientation after photodimerization; neither section gives a −29° base twist, a 36° B-DNA comparison, or an X-ray result for an S-cyanoethyl phosphotriester. Our copy supplies only part of what the sentence attributes to this source (page numbers unavailable). (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [79] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The two T (T5, T6) residues of the CPD in the CPD/GG duplex form wobble base pairs with the opposite G residues, similar to the T6-G15 base pair in the CPD/GA duplex [80].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 5. Differential Effects of CPDs and 6-4PPs on DNA Conformation
What the sources say
- Supportedcites [80] source
The Results and Discussion explicitly state that T5 and T6 in the CPD/GG duplex form wobble pairs with the opposite guanines, similar to the T6·G15 pair in the CPD/GA duplex. (LLM, conf=0.95)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Photolyases seem to be absent or nonfunctional in placental mammals like human [118, 132, 160].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
What the sources say
- Supportedcites [118] source
The Introduction says evidence for active photolyase in placental mammals, including humans, is contradictory and leaves doubt about its existence. The “Photolyase in placental mammals” section reports no human homologue detected by PCR, cites absent photoreactivating activity in human cell extracts, and considers a loss of that activity in placental mammals. These passages support the claim’s cautious wording. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites [132] source
- Not matchedcites [160]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Photoreactivation mediated by the enzyme photolyases is thought to be the major DNA repair pathway in several higher plants such as rice, Arabidopsis, wheat, and maize [170–172].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
What the sources say
- Not matchedcites [170]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites [171] source
- Partly supportedcites [172] sourceExperimental — accuracy not yet measured
The Introduction (p. 1) says photolyase-mediated photoreactivation is thought to be the major repair pathway for two types of UV-induced DNA lesion in higher plants. It does not establish that claim separately for rice, Arabidopsis, wheat, and maize, and the Discussion (p. 5) limits the paper’s own finding to non-proliferating rice leaves rather than DNA repair generally. (LLM, conf=0.84)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Till date, 5,10-methenyltetrahydrofolate (MTHF) [122], 8-hydroxy-5-deaza-riboflavin (8-HDF) [124], and FMN [165] are known as light-harvesting cofactors, which absorb light energy efficiently and transfer them to FADH− [166].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
What the sources say
- Supportedcites [122] sourceExperimental — accuracy not yet measured
Citation [122] is attached specifically to MTHF, not to 8-HDF, FMN, or the energy-transfer statement cited to [166]. The Results identify the native, enzyme-bound folate chromophore in DNA photolyase as MTHF, so this paper supports the identification for which it is cited. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [124] source
- Partly supportedcites [165] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) identifies MTHF, 8-HDF, and FMN as light-harvesting second chromophores and says they transfer absorbed energy to FAD. It does not specify FADH− as the recipient; the photoreactivation assays described in the Results used the radical semiquinone form instead. The claim is supported except for its specific designation of FADH−. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“DSBs can be formed in response to the repair of single strand breaks (SSBs) passing through base excision repair (BER) [94, 95].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 6. UV-Induced DNA Double Strand Breaks
What the sources say
- Partly supportedcites [94] sourceExperimental — accuracy not yet measured
The Background Occurrence of DSBs section says that an unrepaired single-strand break can cause a replication fork to collapse and form a DSB. It does not identify base excision repair as the pathway by which this happens; that specific part of the claim is unsupported by our copy. Page numbers are not available. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites [95] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The splitting of CPD lesion proceeds rapidly within 0.6 nanosecond [167, 178].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
What the sources say
- Supportedcites [167] source
The Results and Discussion states that photolyase has enough time to cleave the cyclobutane ring in 560 ps and describes ring splitting on that timescale. Since 560 ps is 0.56 ns, this supports the cited claim that splitting proceeds within 0.6 ns. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [178] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
- It may state two separate claims as one. 97
- Probably not a substantial claim. 31
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“Recently, it has been reported that the mechanisms of BER and NER (but not photoreactivation) in higher plants are active in proliferating cells [172].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 10. Excision Repair > 10.1. Base Excision Repair (BER)
What the sources say
- Disputedcites [172] sourceExperimental — accuracy not yet measured
The paper supports excision repair in proliferating cells, but explicitly contradicts the exclusion of photoreactivation. The Abstract (p. 1) says both photoreactivation and excision repair are active in proliferating cells; the Discussion (p. 5) likewise says the meristem may need both. (LLM, conf=0.91)
Checked by a reasoning model — may be wrong.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Disputed
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“which is one of the most effective and carcinogenic exogenous agents that can interact with DNA and alter the genome integrity and may affect the normal life processes of all organisms ranging from prokaryotes to mammals [2–10].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 1. Introduction
What the sources say
- Not matchedcites [2]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [3]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites [4] source
- Not matchedcites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites [6] source
- Not checked — no full text of the sourcecites [7] source
- Partly supportedcites [8] sourceExperimental — accuracy not yet measured
The Human health section (page unavailable) links solar UV exposure to skin cancer, while the Aquatic ecosystems section reports UV-associated DNA damage and effects on bacterioplankton. The paper does not establish that UVR is among the most effective carcinogenic agents or that it affects the normal life processes of all organisms from prokaryotes to mammals. (LLM, conf=0.86)
- Partly supportedcites [9] sourceExperimental — accuracy not yet measured
The Introduction reports that UV-B impairs photosynthesis and growth and has harmful effects on plants; the Discussion reports cellular damage in cyanobacteria. Our copy does not establish that UVR is carcinogenic, interacts with DNA or alters genome integrity, or that these effects extend to mammals. (LLM, conf=0.85)
- Partly supportedcites [10] sourceExperimental — accuracy not yet measured
The Introduction (page not supplied) says UVR damages DNA and can inhibit phytoplankton production; the Discussion reports UVR-induced mortality in Mediterranean picocyanobacteria. The paper does not establish that UVR is carcinogenic or extend these effects to all organisms from prokaryotes to mammals. (LLM, conf=0.88)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
Every source the paper cites for this claim was checked and supports it.
In the paper
“One of the transcription factors, TATA-box binding protein (TBP), promotes the selective formation of 6-4PPs in the TATA-box, where the DNA is bent, but CPDs are formed preferentially at the edge of the TATA box and outside where the DNA is not bent [53].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
What the sources say
- Supportedcites [53] source
The Discussion (page not provided) reports that 6-4PP formation was restricted to an internal cluster within the presumed TBP contacts, while other clusters formed CPDs. It also describes the sharp bend induced by TBP; the in vitro results (page not provided) identify CPDs in the flanking regions. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Solar UV radiation is responsible for a wide range of biological effects including alteration in the structure of protein, DNA, and many other biologically important molecules, chronic depression of key physiological processes, and acute physiological stress leading to either reduction in growth and cell division, pigment bleaching, N2 fixation, energy production, or photoinhibition of photosynthe”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 1. Introduction
What the sources say
- Not matchedcites [3]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites [9] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [10] sourceExperimental — accuracy not yet measured
The Introduction (page not provided) describes UV-induced DNA damage, inhibition of primary production, pigment degradation, and changes in nitrogen metabolism; the Discussion reports UV-induced cell mortality. The copy does not support the more specific claims about altered protein structure, chronic versus acute effects, N2 fixation, or reduced energy production. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In all the groups of UVR (i.e., UV-A: 315–400 nm; UV-B: 280–315 nm; UV-C: <280 nm) UV-B radiation produces adverse effects on diverse habitats, even though most of the extraterrestrial UV-B is absorbed by the stratospheric ozone [12].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 1. Introduction
What the sources say
- Partly supportedcites [12] sourceExperimental — accuracy not yet measured
The section on factors affecting surface UV says shorter UV-B wavelengths are particularly sensitive to ozone depletion and that reduced ozone increases damaging radiation for environmental processes (page not provided). This supports the general link between ozone and harmful UV-B, but the copy does not establish that most incoming UV-B is absorbed by stratospheric ozone or document adverse effects across diverse habitats. (LLM, conf=0.78)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Certain UV-absorbing pigments are produced by a number of organisms as a first line of defense; however, they are unable to avoid UV-radiation completely from reaching DNA in superficial tissue [28–32].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 1. Introduction
What the sources say
- Not checked — no full text of the sourcecites [28]
- Not checked — no full text of the sourcecites [29] source
- Not checked — no full text of the sourcecites [30] source
- Partly supportedcites [31] sourceExperimental — accuracy not yet measured
The Marine photoprotective compounds section (page not available) says organisms synthesize or accumulate UV-protective compounds, supporting the claim that such compounds serve as a defense. It does not say they are a 'first line' of defense or that UV radiation can still reach DNA in superficial tissue. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [32] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“A number of endogenous factors such as free radicals [34] generated during metabolic processes as well as exogenous factors such as UV or ionizing radiations [35] are known to interfere with genome integrity.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 2. UV-Induced DNA Damage
What the sources say
- Supportedcites [34] source
The citation to this paper, [34], is attached to the claim about endogenous free radicals, not the separate claim about UV and ionizing radiation cited to [35]. In the section accompanying Figure 1 (page not provided), the paper says the mitochondrial electron transport chain generates reactive oxygen species and that mitochondrial DNA is damaged by them. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites [35] source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“However, Su et al. [61] have reported a new photoproduct of 5-Methylcytosine and Adenine characterized by high-performance liquid chromatography and mass spectrometry.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
What the sources say
- Supportedcites [61] source
The paper’s title identifies it as a report of a new 5-methylcytosine–adenine photoproduct characterized by HPLC and mass spectrometry. The Experimental Procedures sections on RP-HPLC analysis and MS analysis document both methods. (LLM, conf=0.95)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Recently, Rumora et al. [82] have examined the thymine dimer-induced structural changes to the DNA duplex with several small, base-selective reactive chemical probes.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 5. Differential Effects of CPDs and 6-4PPs on DNA Conformation
What the sources say
- Supportedcites [82] source
The paper’s Discussion, under “Examining the Structure of Lesion-Containing DNA with Small Reactive Probes,” says the authors probed lesion-containing DNA with small reactive molecules and identifies KMnO4, DEPC, and DMS as the probes selected to examine base pairing and stacking. The Results section identifies the lesion studied as a central thymine dimer in a DNA duplex. (LLM, conf=0.95)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“UV-induced DNA lesions such as CPDs and 6-4PPs show differential effects on DNA conformation, impairing their regulatory functions and other dynamic processes [24, 26, 75, 76].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 5. Differential Effects of CPDs and 6-4PPs on DNA Conformation
What the sources say
- Not checked — no full text of the sourcecites [24] source
- Partly supportedcites [26] sourceExperimental — accuracy not yet measured
The Figure 1 discussion reports different effects of the (6–4) adduct and the Dewar product on DNA distortion and polymerase bypass; the Abstract says UV photoproducts can block replication. The comparison in this source is not between CPDs and 6-4PPs, and the passages do not support the claim about impaired regulatory functions. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [75] source
- Not matchedcites [76]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“the existence of repair mechanisms was observed by Kelner [154] and Dulbecco [155] independently.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 8. DNA Repair
What the sources say
- Partly supportedcites [154] sourceExperimental — accuracy not yet measured
The Discussion reports Kelner’s observation that visible light restored viability to UV-irradiated cells and proposes restoration of an altered cellular constituent as a working hypothesis. It does not identify that constituent as DNA or establish a DNA repair mechanism; it also does not address whether Dulbecco’s observation was independent. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [155] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“To avoid the deleterious effects of UVR, plants have acquired two main protective strategies; shielding by flavonoids and phenolic compounds [168, 169] and DNA repair by photoreactivation.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
What the sources say
- Partly supportedcites [168] sourceExperimental — accuracy not yet measured
The paper’s Results (page not supplied) show that flavonoid-containing maize tissue had less UV-induced DNA damage, supporting flavonoid shielding. Our copy does not establish shielding by phenolic compounds beyond flavonoids. The citation is attached to the shielding clause, not the subsequent photoreactivation clause. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [169] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Deprotonated reduced flavin adenine dinucleotide (FADH−) is found in all known photolyases as a catalytic cofactor, which transfers energy in the form of an electron to the CPD, splitting the cyclobutane ring with the generation of two monomeric bases [157, 167]”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
What the sources say
- Not checked — no full text of the sourcecites [157] source
- Supportedcites [167] source
The paper describes fully reduced FADH− as photolyase’s catalytic cofactor and says the excited cofactor transfers an electron to the pyrimidine dimer, whose ring then splits (Abstract). The Results and Discussion report direct electron transfer and electron return from repaired thymine monomers. Its general description of photolyase supports the citing sentence’s broad cofactor statement, although the experiments used E. coli photolyase. (LLM, conf=0.89)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The CSA protein (44 kDa) which belongs to “WD repeat” family of proteins exhibits structural and regulatory roles and CSB proteins (168 kDa) which belong to SWI/SNF family of proteins exhibit DNA-stimulated ATPase activity [217–219].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [217] source
- Not checked — no full text of the sourcecites [218] source
- Supportedcites [219] source
The introductory passage gives CSA as a 44 kDa WD-repeat protein and CSB as a predicted 168 kDa SWI/SNF protein. The Discussion describes structural and regulatory roles for the WD-repeat family, and the paper reports DNA-stimulated ATPase activity for CSB. No page numbers are available in our copy. (LLM, conf=0.90)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“hHR23B-XPC complex or only XPC exhibits a similar high affinity for both UV-induced single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) [230, 259], preferentially binds to DNA with various lesions [259] and even to small bubble structures with or without a lesion [260].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Partly supportedcites [230] sourceExperimental — accuracy not yet measured
The Results report that the XP-C–HHR23B complex bound strongly to a single-stranded DNA-cellulose column. The Discussion says this indicates high affinity for ssDNA but explicitly leaves open which component is responsible. The paper does not establish similarly high affinity for UV-damaged double-stranded DNA or for XPC alone; the citing sentence assigns the lesion and bubble claims to other references. (LLM, conf=0.88)
- Partly supportedcites [259] sourceExperimental — accuracy not yet measured
The DNA Binding Properties section (page not supplied) reports comparable high-affinity binding of the XPC–HHR23B complex to single- and double-stranded DNA, with slightly higher affinity for UV-irradiated duplex DNA; XPC alone also binds DNA strongly. It does not establish comparable binding to UV-damaged DNA in both strand forms or a preference for DNA with various kinds of lesions. The bubble-structure claim is attached to a different citation, [260], so it is not assessed against this paper. (LLM, conf=0.89)
- Supportedcites [260] source
The citation to this paper is attached to the small-bubble claim. In the section “XPC-HR23B binds a small bubble structure regardless of the presence or absence of lesions,” the authors report efficient binding to 3- and 5-base bubbles without AAF damage and binding to a 3-base bubble regardless of whether the lesion is present. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“hHR23B-XPC is absolutely required for dual incision as well as for open complex formation during GG-NER [243, 261].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Partly supportedcites [243] sourceExperimental — accuracy not yet measured
In “XPC and XPA participate in open complex formation,” XPC-defective extracts failed to form the full open complex around a platinum lesion, and adding XPC-hHR23B restored both opening and dual incision. The same section says that repair of certain other lesions does not require XPC in vitro, so the paper does not support “absolutely required” as an unqualified statement about GG-NER. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites [261] source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Both XPA and RPA can recruit with the DNA lesions in absence of XPG, and similarly XPG can also join the damage sites in the absence of XPA [238, 239].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [238] source
- Partly supportedcites [239] sourceExperimental — accuracy not yet measured
The introduction (page unavailable) says XPA binds preferentially to damaged DNA, and the paper reports an XPA–RPA interaction. It does not establish that XPA or RPA is recruited to lesions without XPG, or that XPG reaches damage sites without XPA. (LLM, conf=0.82)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Both hHR23A and -B harbor a ubiquitin-like moiety at their amino terminus [230].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Supportedcites [230] source
Figure 7B compares the N-terminal conserved regions of HHR23A and p58/HHR23B with ubiquitin-like domains. The text also identifies a ubiquitin-like N-terminus in the RAD23 homologues. Page numbers are not provided in our copy. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Overall, it has been distinguished that RNA pol II with the recruitment of two proteins (i.e., CSA and CSB) proceeds the TCR while hHR23B-XPC complex is the first factor in NER that initiates GGR by sensing and binding lesions, locally distorting the DNA double helix and recruiting the other factors of the system [227].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Supportedcites [227] source
The paper states that elongating RNA polymerase II detects lesions in transcription-coupled NER and that CSA and CSB are needed for efficient repair of transcribed strands. In the XPC-hHR23B section, it explicitly says the complex initiates global-genome NER by binding lesions, distorting the helix locally, and recruiting other repair factors. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Genetic and genomic analysis indicates that plant NER pathway is homologous to that of mammals and fungi and unrelated to the bacterial system [204, 271–273].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [204] source
- Partly supportedcites [271] sourceExperimental — accuracy not yet measured
The Results (page not specified) identify plant homologs of eukaryotic NER genes, and the Discussion (page not specified) concludes that the repair pathway is highly conserved among plants, mammals, and fungi. But the Results describe the bacterial mechanism as similar, with little homology between bacterial and eukaryotic proteins; that does not support calling the systems wholly unrelated. (LLM, conf=0.84)
- Not matchedcites [272]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [273]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For instance, 6-4PPs are removed much faster from the genome than CPDs, possibly because of disparity in affinity of the damage sensor hHR23B-XPC.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Partly supportedcites [211] sourceExperimental — accuracy not yet measured
The Introduction and results on repair in specific sequences (page not supplied) report that 6-4PPs are repaired much faster than CPDs in normal human fibroblasts. The Discussion reports similar repair kinetics for the two lesions in XP-C fibroblasts. Our copy does not support the proposed explanation involving differential affinity of hHR23B-XPC. (LLM, conf=0.88)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- The authors state this as an assumption: XPC preferentially binds single-stranded DNA in the non-damaged strand opposite a lesion.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“XPC is the sole XP factor not essential for TCR and is restricted to GGR [211].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Partly supportedcites [211] sourceExperimental — accuracy not yet measured
The Introduction says XP-C fibroblasts retain transcription-coupled repair (TCR), and the Discussion contrasts their TCR-only repair with normal cells’ TCR and global repair. This supports that XPC is not essential for TCR and is associated with global repair, but the paper does not establish that XPC is the sole XP factor with that distinction. (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Rad51 (a functional homolog of the E. coli RecA) [298] is the central protein in HR, binds the exposed single-stranded tails forming a nucleoprotein filament and this early step is promoted by a Rad55/Rad57 protein heterodimer [299] by overcoming the inhibitory effects of the heterotrimeric single-stranded DNA binding protein RPA [300].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
What the sources say
- Could not verifycites [298] sourceExperimental — accuracy not yet measured
Citation [300] is attached to the claim that Rad55/Rad57 overcomes RPA’s inhibition of Rad51 filament formation. The paper’s passage labeled Abstract (page unavailable) says RPA binding is essential for Rad51 loading, but does not address that proposed inhibitory effect or how Rad55/Rad57 might overcome it. Searches for Rad55/Rad57 and RPA inhibition found no decisive passage. (LLM, conf=0.73)
- Not checked — no full text of the sourcecites [299] source
- Not matchedcites [300]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“It has been shown that Ku complex (a heterodimer of Ku70/Ku80 [≈86]) is a major end binding factor in mammalian cells, possess end bridging activity [308, 309].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.2. Non-Homologous End Joining
What the sources say
- Not checked — no full text of the sourcecites [308] source
- Supportedcites [309] source
The Introduction identifies Ku as a heterodimer of 70 and 86 kDa subunits that binds duplex-DNA ends and is implicated in mammalian end joining. The ‘Ku promotes association of two DNA molecules’ section reports a pulldown assay showing that Ku bridges DNA molecules, while the Discussion describes its role in end joining as a critical component of its function in vivo. The copy does not quantify ‘major,’ but it supports the broad characterization. (LLM, conf=0.89)
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The eukaryotic RAD51s play a significant role in HR, maintaining genome integrity in both mitotic as well as meiotic cell cycle [288, 289].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
What the sources say
- Not checked — no full text of the sourcecites [288] source
- Partly supportedcites [289] sourceExperimental — accuracy not yet measured
The Abstract (page not available) says Rad51 plays a central role in homologous recombination, and the discussion of RAD51-paralog mutants reports chromosomal aberrations alongside impaired Rad51-mediated recombination. The paper identifies DMC1 as meiosis-specific, but the passages do not establish that RAD51 proteins maintain genome integrity in both mitotic and meiotic cell cycles; that part of the claim is more specific than the evidence. (LLM, conf=0.82)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Genetic and biochemical evidence suggest that Mre11-Rad50-Xrs2 (MRX) act as end bridging factor in yeast NHEJ, since DNA-PKcs is absent in them [319, 320].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.2. Non-Homologous End Joining
What the sources say
- Partly supportedcites [319] sourceExperimental — accuracy not yet measured
The Discussion’s “A DNA End-Bridging Model” proposes that Mre11, or the MRX complex, holds two DNA ends together; the Discussion also cites yeast genetic and biochemical observations linking MRX to NHEJ. Our copy does not say that DNA-PKcs is absent in yeast or give its absence as the reason MRX may bridge ends. Page numbers were not available in the indexed passages. (LLM, conf=0.88)
- Not matchedcites [320]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Moreover, a plant homologue of human NER gene of the endonuclease, ERCC1, has been cloned from Lilium longiflorum which showed a similar role in DNA repair in plants [279].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Partly supportedcites [279] sourceExperimental — accuracy not yet measured
The Isolation of cDNA clone and sequence analysis section identifies a Lilium longiflorum clone homologous to human ERCC1. The DNA repair activity section shows that lily ERCC1 corrected sensitivity to mitomycin C in ERCC1-deficient hamster cells, but did not correct UV sensitivity. The paper infers a conserved DNA-repair role in plants; it does not demonstrate that role in plant cells, as the claim's 'showed' implies. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“SOS repair system is initiated by interaction of two crucial proteins the RecA and the LexA repressor which curbs the expression of SOS genes by binding to their promoters [327] (Figure 14).”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 13. SOS Repair/Response
What the sources say
- Supportedcites [327] source
The Results and discussion section (‘4 – Other repair related proteins,’ subsection ‘A – SOS system’) says LexA represses SOS genes by binding their promoters and that RecA inactivates LexA to induce the system. This supports the cited description of how SOS repair is initiated. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The recA gene encodes a DNA-dependent ATPase that binds to ssDNA and promotes strand invasion and exchange between homologous DNA molecules [285].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
What the sources say
- Supportedcites [285] source
The introductory passage identifies recA protein as the product of the recA gene and says it promotes assimilation of single-stranded DNA into homologous duplex DNA, forming a D-loop. The Results describe recA binding to single-stranded DNA, and the abstract reports ATP hydrolysis catalyzed by recA in its presence. Page numbers are not available in our copy. (LLM, conf=0.91)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“When the repair mechanisms are unsuccessful, it may cause cellular senescence (permanent cell cycle arrest), oncogenesis or apoptosis [354].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 14. Cell-Cycle Checkpoint Activation
What the sources say
- Partly supportedcites [354] sourceExperimental — accuracy not yet measured
The Introduction (page not specified) says cells with damage beyond repair may undergo apoptosis. It does not identify senescence or oncogenesis as outcomes of failed repair; the section on malfunctioning apoptosis links cancer to faulty apoptosis instead. (LLM, conf=0.86)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Recently, the genes imuA and imuB have been described that induce SOS mutagenesis in Caulobacter crescentus, but absent in E. coli [332].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 13. SOS Repair/Response
What the sources say
- Partly supportedcites [332] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) states that the SOS-regulated imuAB–dnaE2 operon is responsible for most damage-inducible mutagenesis in Caulobacter crescentus. It contrasts this machinery with that of E. coli, but the passages do not establish that both imuA and imuB are absent from E. coli. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The occurrence of DNA damage response in G2-phase, leads to checkpoint mediator (claspin) dependent activation of Chk1/2, followed by SCFβTrcP mediated degradation of CDK-activating phosphatase Cdc25A [341, 342], that results in arrest of multiple cell-cycle transition including the G2 checkpoint [343, 344].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 14. Cell-Cycle Checkpoint Activation
What the sources say
- Partly supportedcites [341] sourceExperimental — accuracy not yet measured
The Abstract and Discussion (page not provided) support SCFβ-TRCP-mediated Cdc25A turnover in response to DNA damage and Chk1-dependent Cdc25A ubiquitination. They do not establish claspin-dependent Chk1/2 activation specifically in G2 phase. The sentence attaches separate citations to its later claim about arresting multiple cell-cycle transitions. (LLM, conf=0.86)
- Partly supportedcites [342] sourceExperimental — accuracy not yet measured
The introductory passage (page unavailable) says that DNA damage activates Chk1 and Chk2, promoting SCF-dependent Cdc25A degradation, and describes β-TrCP-dependent ubiquitination. It does not establish that this response occurs specifically in G2 or that Chk1/2 activation depends on claspin. The cell-cycle-arrest clause has separate citations [343, 344] and is not assessed against this source. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites [343] source
- Partly supportedcites [344] sourceExperimental — accuracy not yet measured
The Results report that DNA damage induced G2 arrest with proteasome-dependent Cdc25A destruction, and that restoring Cdc25A partially abrogated the G2 checkpoint. The Introduction also describes Chk1- or Chk2-mediated Cdc25A phosphorylation in earlier checkpoint responses. Our copy does not establish claspin-dependent Chk1/2 activation or identify SCFβTrcP as the mediator of Cdc25A degradation. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“It has been reported that translesion synthesis past a CPD, facilitated by pol. η, with the insertion of adenines opposite both bases of a T∧T CPD [352], where as 6-4TT may lead to a G insertion.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 14. Cell-Cycle Checkpoint Activation
What the sources say
- Supportedcites [352] source
The citation is attached to the CPD clause, not the subsequent 6-4TT clause. In the translesion-synthesis section (p. 3102), the paper reports that polymerase η efficiently bypassed a TT CPD; its discussion reports preferential dAMP incorporation opposite the thymines of a CPD and preferential extension from primers with A opposite a dimer thymine. The paper presents the dAMP-incorporation result as a finding from steady-state kinetic experiments, rather than as a determination made in its own incorporation assay. (LLM, conf=0.90)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Interestingly, it has been found that DNA polymerase IV (dinB) is also involved in translesion synthesis in E. coli [331].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 13. SOS Repair/Response
What the sources say
- Partly supportedcites [331] sourceExperimental — accuracy not yet measured
The Results identify dinB as E. coli DNA polymerase IV, and the Discussion links it to spontaneous mutation when replication is stalled. Neither passage establishes that it performs translesion synthesis; the paper discusses mutation on ostensibly undamaged templates instead. (LLM, conf=0.82)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Additionally, double-strand break repair (by homologous recombination and nonhomologous end joining), SOS response, cell-cycle checkpoints, and programmed cell death (apoptosis) are also operative in various organisms with the expense of specific gene products.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > Abstract
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The hydrolytic deamination (loss of an amino group) can directly convert one base to another; for example, deamination of cytosine results in uracil and at much lower frequency adenine to hypoxanthine.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 2. UV-Induced DNA Damage
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“The formation of “spore photoproduct” has been detected in UV-irradiated bacterial spores by the addition of methyl group of one thymine residue to the C5 position of an adjacent thymine. In most cellular environments, there is no much significance of this photoproduct, since it requires anhydrous conditions for its formation [49].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
What the sources say
- Not checked — no full text of the sourcecites [49] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The 6-4PPs are eagerly converted into their Dewar valence isomers upon exposure to UV-B or UV-A radiation that may further undergo reversion to the 6-4PPs upon exposure to short-wavelength UV radiation [45].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
What the sources say
- Not checked — no full text of the sourcecites [45] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Although UV-B radiation has less than 1% of total solar energy, it is a highly active component of the solar radiation that brings about chemical modification in DNA and changes its molecular structure by the formation of dimers.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 1. Introduction
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Certain enzymes, such as superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), and scavengers such as vitamin C, B, and E, cysteine, and glutathione play an additional role in defense against UV radiation [33].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 1. Introduction
What the sources say
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“The amounts of CPDs and 6-4PPs are about 75 and 25%, respectively, of the total UV-mediated DNA damage products [22]; however, the ratio between the yield of CPDs and 6-4PPs mainly depends upon the two adjacent bases involved in the formation of dimers [54].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
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In the paper
“Moreover, ozone depletion followed by increased UV exposure has been predicted to continue throughout most of this century [11].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 1. Introduction
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In the paper
“It has been demonstrated that the main photoproducts are cis-syn-configured CPD lesions, while trans-syn-configured CPD lesions are formed in much less quantity [47].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
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In the paper
“In depurination/depyrimidination, there are complete removals of purine/pyrimidine bases, leaving the deoxyribose sugar depurinated/depyrimidinated, that may cause breakage in the DNA backbone.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 2. UV-Induced DNA Damage
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“Thus the heterogeneous distribution of the UV-induced photolesions in the DNA depends on the sequences that facilitate DNA bending as well as the chromatin modulation through the binding of specific protein [55].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
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“CPDs correspond to the formation of a four-member ring structure involving C5 and C6 of both neighboring bases whereas 6-4PPs are formed by a noncyclic bond between C6 (of the 5′-end) and C4 (of the 3′-end) of the involved pyrimidines via spontaneous rearrangement of the oxetane (when the 3′-end is thymine) (Figure 3(a)) or azetidine (when the 3′-end is cytosine) (Figure 3(b)) intermediates [5, 44”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
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In the paper
“DNA damage results in (i) misincorporation of bases during replication process, (ii) hydrolytic damage, which results in deamination of bases, depurination, and depyrimidination [36], (iii) oxidative damage, caused by direct interaction of ionizing radiations (IR) with the DNA molecules, as well as mediated by UV radiation-induced free radicals or reactive oxygen species [37, 38], and (iv) alkyl”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 2. UV-Induced DNA Damage
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“One of the most prominent targets of solar UV-radiation is cellular DNA, which absorbs UV-B radiation and causes adverse effects on living systems such as bacteria [15, 16], cyanobacteria [17], phytoplankton [18], macroalgae [19], plants [20], animals, and humans [21–23].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 1. Introduction
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“At high concentrations oxygen-free radicals or, more frequently, reactive oxygen species (ROS) can induce damage to cell structure, lipids, proteins as well as DNA and results in oxidative stress which has been implicated in a number of human diseases [40].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 2. UV-Induced DNA Damage
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In the paper
“CPDs are formed at higher quantity by cycloaddition reaction between two pyrimidine bases [47] in single-stranded DNA (ssDNA) and at the flexible ends of poly (dA)-(dT) tracts, but not at their rigid centre [50, 51].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
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In the paper
“UV-C radiation is quantitatively absorbed by oxygen and ozone in the Earth's atmosphere, hence does not show much harmful effects on biota.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 1. Introduction
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In the paper
“It has been documented that UV-B severely affects survival, fecundity, and sex-ratio in several intertidal copepods [14].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 1. Introduction
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In the paper
“In double stranded B-DNA, where the dimer entails two adjoining pyrimidine bases on the same DNA strand, only the syn isomers can be generated, whereas the cis isomer is preferred over the trans isomer to a great extent [42].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
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In the paper
“Photodimerization of adenine (A) involves the cycloaddition of N7-C8 double bond of the 5′-A across the C6 and C5 positions of the 3′-A [65, 69] and generates a very unstable azetidine intermediate.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 4. UV-Induced Purine Photoproducts
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In the paper
“There is little information concerning the formation of cytosine hydrates in UV-irradiated DNA due to instability of the resulting photoproduct [63].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 3. UV-Induced Pyrimidine Photoproducts
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In the paper
“Overall, it has been concluded that UV-induced DNA lesions such as CPDs, 6-4PPs, abasic site, strand breaks, and oxidative product are the predominant and most persistent lesions and if not repaired may cause severe structural distortions in the DNA molecule, thereby affecting the important cellular processes such as DNA replication and transcription, compromising cellular viability and functional”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 4. UV-Induced Purine Photoproducts
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In the paper
“Although dipyrimidine photoproducts are the preferential outcome of UV-B radiation, the biological importance of UV radiation-induced modifications of DNA purine bases has also been recognized [64].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 4. UV-Induced Purine Photoproducts
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In the paper
“UV-B-induced ROS [89] as well as DNA lesions (CPDs and 6-4PPs) may cause primary as well as secondary breaks, respectively.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 6. UV-Induced DNA Double Strand Breaks
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In the paper
“The extent of adenine-containing photoproduct (A-T) is very low (1 × 10−5 in native DNA) but these lesions may contribute to the biological effects of UV radiation in view of the fact that the A-T adduct has been shown to be mutagenic [67, 68].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 4. UV-Induced Purine Photoproducts
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In the paper
“DNA photolyases (45–66 kDa) having 420–616 amino acid residues [158] are monomeric flavin-dependent repair enzymes, consisting of two known cofactors, a catalytic cofactor and a light-harvesting cofactor.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
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In the paper
“The process of photoreactivation is executed by means of a photoreactivating enzyme known as “photolyase”, which is well conserved and found throughout the three domains of life (Table 2).”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
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“6-4 photolyases have been identified in certain organisms like Drosophila, silkworm, Xenopus laevis, and rattle snakes [22].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
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In the paper
“CPD photolyases have been reported in diverse groups such as archaea, bacteria, fungi, virus, plants, invertebrates, and many vertebrates including aplacental mammals (Table 2).”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
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In the paper
“It has been observed that about 240 KJ/mol of energy is captured upon absorption, out of which about 125 KJ/mol energy is consumed during the initial electron transfer from the excited FADH to CPD lesions [177].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
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In the paper
“UV-induced replication arrest in the xeroderma pigmentosum variant (XPV) followed by the accumulation of Mre11/Rad50/Nbs1 complex and phosphorylated histone H2AX (γ-H2AX) in large nuclear foci at sites of stalled replication forks also suggests that UV damage leads to the formation of DSBs during the course of replication arrest [90, 95].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 6. UV-Induced DNA Double Strand Breaks
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- The authors state this as an assumption: Initial UV photoproducts are converted into DNA double-strand breaks during replication through collapse of replication forks.
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In the paper
“The enzyme binds specifically to the CPDs (CPD photolyase) or 6-4PPs (6-4 photolyase) and directly monomerizes the cyclobutane ring of the pyr <> pyr, using the energy of visible/blue-light and protects the genome from deleterious effects of UVR [157, 158].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
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In the paper
“Studies on Arabidopsis seedling, rice, and alfalfa indicate that photoreactivation greatly enhances the rate of removal of dimers, although, in the absence of photoreactivating (blue) light, dimers are slowly eliminated from bulk DNA and 6-4PPs are generally observed to be repaired more quickly than CPDs [173, 174].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
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In the paper
“A number of workers have identified a human photolyase which shows homology with Cry gene (plant blue-light receptor) and about 40% sequence identity to the Drosophila 6-4 photolyase”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
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In the paper
“Overall, it seems that UV radiation does not directly produce DNA DSBs but rather produces pyrimidine dimers and other photoproducts leading to replication arrest and DSBs.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 6. UV-Induced DNA Double Strand Breaks
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- The authors state this as an assumption: Initial UV photoproducts are converted into DNA double-strand breaks during replication through collapse of replication forks.
In the paper
“MacFarlane and Stanley [178] have suggested that photolyase enzyme is indeed left in the semiquinonid state after accomplishment of repair of the CPD lesion.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 9. Photoreactivation
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In the paper
“Recently, Almeida and Sobol [184] have proposed a unified model of SP-BER and LP-BER.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 10. Excision Repair > 10.1. Base Excision Repair (BER)
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In the paper
“Eukaryotic NER is known to be similar to prokaryotes regarding the biochemical strategy used but differs widely in the nature and number of proteins used [210].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 10. Excision Repair > 10.2. Nucleotide Excision Repair (NER)
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In the paper
“The AP-site is removed by the action of AP endonuclease-1 (APE-1) along with phosphodiesterase that breaks the DNA strand along 5′ or 3′ to the AP site, respectively, and subsequently the gap is filled by a repair DNA polymerase and the strand is joined by a DNA ligase (Figure 10) [182, 191].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 10. Excision Repair > 10.1. Base Excision Repair (BER)
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In the paper
“Discovery of NER was first described in E. coli [212, 213] where about six proteins such as UvrA, B, and C (known as ABC-complex, which shows excinuclease activity), UvrD (helicase II), DNA polymerase I (pol. I), and DNA ligase are recruited to complete the repair [214, 215].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 10. Excision Repair > 10.2. Nucleotide Excision Repair (NER)
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In the paper
“DNA having one nucleotide lesion is removed by short-patch BER (SP-BER) whereas two/more nucleotide lesion is repaired by long-patch BER (LP-BER) pathway [195] (Figure 10).”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 10. Excision Repair > 10.1. Base Excision Repair (BER)
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In the paper
“The flap endonuclease (Fen1) protein then displaces the ensuing DNA flap leaving a nick which is ligated by DNA ligase I (Lig. I) [200, 201].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 10. Excision Repair > 10.1. Base Excision Repair (BER)
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In the paper
“The formation of AP sites has been observed in seeds of Zea mays during early germination. This phenomenon was attributed to the action of DNA glycosylases on lesions accumulated during seed storage [207], implying the presence of BER in this species.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 10. Excision Repair > 10.1. Base Excision Repair (BER)
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In the paper
“Unlike SP-BER, LP-BER involves proliferating cell nuclear antigen (PCNA) coupled with DNA pol. −δ/ε or β which extends and fills the gap by inserting 2–13 nucleotide [184].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 10. Excision Repair > 10.1. Base Excision Repair (BER)
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In the paper
“It has been suggested that the RNA pol II backs up some nucleotides upon encountering the lesion to facilitate the accessibility of the repair machinery to the lesion site [220, 221].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
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- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“It is expected that the CSB protein ubiquitinates the stalled elongating RNA pol II complex at the lesion and enhances the assembly of repair factors [222].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [222] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Recently, Fousteri et al. [224] has revealed that CSB is a prerequisite factor in vivo to assemble NER proteins while it is not essential to recruit TFIIH or NER complex in vitro.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [224] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“TFIIH is usually involved in initiation of RNA Pol II transcription, but upon DNA damage can be employed in cell cycle regulation and NER (both in global genome and TC-NER) [228, 235].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In mammalian cells, the quantity of hHR23B is higher than the XPC [255]”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [255] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Sugasawa et al. [226] showed that hHR23B-XPC attaches directly to DNA damage and alters the DNA conformation around the lesion.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [226] source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“TFIIH is a ten-subunit protein complex (Table 4) composed of a core complex (XPB, XPD, p62, p44, p34, p52, p8) and of a cdk activating kinase (CAK) subunit (Mat1, Cdk7, CyclinH) [236].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [236] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“XPA and heterotrimeric replication protein A (RPA; RPA70, 32 and 14) are recruited to confirm the presence of DNA damage and form a more stable preincision complex [185].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [185] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“It has been found that the XPD helicase activity is dispensable for in vitro transcription [262] but seems to play an additional architectural role within the complex by connecting the core TFIIH with the CAK subunit [228, 236].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“very recently it has been reported that mostly ligase III, in cooperation with its partner XRCC1 seals the DNA nicks and ligase I plays a minor role in actively replicating cells, but not in quiescent cells [268].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [268] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Several observations provide evidence that “dark” repair of UV-induced NER is a significant DNA repair mechanisms in plants that is capable of excising dimers, particularly 6-4PPs [30, 270].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“It was shown that DDB complex is recruited first to the lesion (CPD) before the XPC complex, on little distorted DNA helix; however, in case of large distortion of the DNA helix caused by 6-4PPs, direct recognition by XPC is also possible for this”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“It was reported that XPC and UV-DDB materialize to assist for the efficient recognition of UV-induced photolesions and that both factors are ubiquitylated [250, 253].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Lesions that cause little distortion can be recognized by the DDB complex which is also part of an E3 ubiquitin (Ub) ligase that poly-ubiquitinates XPC and XPE [216].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [216] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A UV-specific endonuclease resembling UvrABC nuclease in activity was partially characterized from spinach [206].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
- Not checked — no full text of the sourcecites [206] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“XPG, which belongs to flap endonuclease-1 (FEN-1) family of structure-specific endonucleases [264], is not only involved in performing the 3′ incision in NER but also required for stabilizing the fully open DNA bubble structure and to permit the 5′ incision by ERCC1- XPF [265].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 11. Mechanistic Differences between GG- and TC-NER in Mammalian Cells
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Recombinational repair is a significant UV-tolerance mechanism in plants where UV-induced chromosomal rearrangements including homologous intrachromosomal recombination events have been found [296].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
What the sources say
- Not checked — no full text of the sourcecites [296] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In E. coli, this HJ is resolved by the positioning of RuvABC resolvasome, however in eukaryotic cell, how this HJ is resolved to give crossover products is not known.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The accumulation of massive amount of DNA lesions within the cells under different specific physiological responses [324] may lead to the occurrence of SOS repair system which was well described in E. coli, where the involvement of more than 40 genes have been found [325].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 13. SOS Repair/Response
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“When HR is inactivated, an alternate pathway, that is, NHEJ becomes operative for the repair of DSBs [303], that also involves a multi-protein complex and has been found in organisms ranging from a few prokaryotes to mammals.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.2. Non-Homologous End Joining
What the sources say
- Not checked — no full text of the sourcecites [303] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Homologues of most of the genes are highly conserved among all eukaryotes including human [282, 283] highlighting these genes for cell survival.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The proteolytic activity of RecA protein inactivates the LexA repressor and induces all the genes to which LexA is associated.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 13. SOS Repair/Response
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For instance, mutation of at least one of these repair proteins, called BRCA1 may lead to hereditary breast cancer [280].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair
What the sources say
- Not checked — no full text of the sourcecites [280] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Among all, E. coli recA gene and its eukaryotic homologs RAD51s are the best recombination genes [284].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
What the sources say
- Not checked — no full text of the sourcecites [284] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The Rad51 nucleoprotein filament in association with other repair protein searches the genome for an intact copy of the broken DNA on the sister chromatid to form a heteroduplex joint molecules or D-loop that is matured in to a Holliday junctions (HJs). HJ is then resolved to give crossover products (Figure 13).”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Virtually, the joint molecule formation is followed by extension of the incoming strand by DNA polymerases and branch migration, leading to restoration of the genetic information [283, 302].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Among eukaryotes, the yeast S. cerevisiae and Schizosaccharomyces pombe have four RAD51-like genes (RAD51, DMC1, RAD55/rhp55, and RAD57/rhp57) [286, 287] whereas vertebrate animals and plants have seven types of RAD51-like genes (RAD51, -51B, -51C, -51D, DMC1, XRCC2, and XRCC3) [288].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“There are 59% identity between S. cerevisiae, human and mouse in the case of Rad51 protein (Rad51p) and 30% identity to RecA protein of bacteria [290], whereas yeast and human proteins are 60% identical in case of Rad52 proteins (Rad52p) [291].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.1. Homologous Recombination
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“It has been suggested that as in mammals, breaks are repaired by nonhomologous recombination far more frequently than via HR [202, 323].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.2. Non-Homologous End Joining
What the sources say
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“DSB repair through HR process is an error free pathway, since, it requires an extensive region of sequence homology between the damaged and template strands, whereas NHEJ is an error prone, alternate pathway for the repair of DSBs, essentially joins broken chromosomal ends independent of sequence homology.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Recently, a third protein, designated as XLF or Cernunnos [313] that has homology to Xrcc4, has been identified and shown to co-associate with the DNA ligaseIV/Xrcc4 complex [314, 315].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 12. Recombinational Repair > 12.2. Non-Homologous End Joining
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The intermediate component of this pathway is β-TrcP (an adaptor protein) that links both WEE1 [346] and claspin [347–349] with the SCF ubiquitin ligase complex and this SCFβTrcP acts as trigger of checkpoint initiation where recognition of phosphodegron β-TrcP is exposed after Chk1 mediated Phosphorylation of Cdc25A [350], as well as checkpoint recovery which is linked with Plk1 mediated Phospho”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 14. Cell-Cycle Checkpoint Activation
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Under normal conditions, this latter complex being active promotes G2/M transition and upon inactivation due to DNA damage, blocks the G2 cell-cycle and unlike the G1/S checkpoint this arrest seems to be partly p53/p21 independent [183].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 14. Cell-Cycle Checkpoint Activation
What the sources say
- Not checked — no full text of the sourcecites [183] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Activation of both ATM and ATR results in phosphorylation of Chk2 and Chk1 respectively which transfer the DNA damage signal to the cell-division cycle proteins Cdc25(A-C).”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 14. Cell-Cycle Checkpoint Activation
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“It has been shown that ATM and DNA-PK are activated by the presence of DSBs where as activation of ATR takes place by single strand regions of DNA [337, 338].”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 14. Cell-Cycle Checkpoint Activation
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The SOS response is induced with damage signal but it is highly mutagenic due to engagement of error-prone DNA polymeraseV (UmuC/UmuD2 complex) [329] and DNA polymerase IV [330] in E. coli.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 13. SOS Repair/Response
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Majchrzak et al. [324] examined the effects of SOS response on genome stability of trinucleotide repeat sequences (TRS) in E. coli and observed that SOS response genes destabilized the TRS tracts and also altered the superhelical density of the plasmids.”
§ Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair > 13. SOS Repair/Response
What the sources say
- Not checked — no full text of the sourcecites [324] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The authors state this as an assumption.
Initial UV photoproducts are converted into DNA double-strand breaks during replication through collapse of replication forks.
“It was assumed that initial photoproducts are converted into DSBs during DNA replication, due to not a distinct process, that is, “collapse of replication forks” [93].”
The paper relies on this without support.
DNA stability is essential for the proper functioning and existence of all living systems.
“DNA is one of the prime molecules, and its stability is of utmost importance for proper functioning and existence of all living systems.”
The paper relies on this without support.
Solar UVR-induced DNA damage is a key event that strongly affects normal life processes in all organisms.
“Induction of DNA damage by solar UVR is a key event that drastically influences the normal life processes of all organisms.”
The authors state this as an assumption.
Most base excision repair is carried out by the short-patch subpathway, started by either a monofunctional or a bifunctional glycosylase.
“It is assumed that majority of repair takes place through SP-BER, initiated either by monofunctional or by bifunctional glycosylase [184].”
The authors state this as an assumption.
Transcription-coupled nucleotide excision repair is initiated when RNA polymerase II encounters a lesion.
“It is assumed that TC-NER proceeds when the transcription machinery RNA pol II encounters a lesion.”
The authors state this as an assumption.
XPC preferentially binds single-stranded DNA in the non-damaged strand opposite a lesion.
“It is supposed that XPC binds preferentially to the stretch of ssDNA that occurs in the nondamaged strand, opposite to a lesion [252].”
The authors state this as an assumption.
hHR23A can replace hHR23B in forming a complex with XPC and in stimulating XPC repair activity.
“It has been assumed that hHR23A can substitute for hHR23B in complex formation and stimulation of XPC repair activity [258].”
The authors state this as an assumption.
RPA binds the undamaged strand of the opened DNA bubble, positioning and stimulating the endonuclease activities of XPG and ERCC1-XPF.
“It was assumed that RPA binds the nondamaged strand of the opened DNA bubble, thus allowing exact positioning and stimulation of the endonuclease activities of XPG and ERCC1-XPF [246, 247].”
The authors state this as an assumption.
DNA ligase I seals the remaining nick after repair synthesis.
“It is assumed that ligase-I is responsible for ligation of remaining nick [267]”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“6-4PP lesions cause a more pronounced distortion on the DNA molecule, i.e. generating a 44° bend of the DNA helix, contrasting to a 9° helix bend caused by CPDs ( 3 , 27 )”
From Photorepair of Either CPD or 6-4PP DNA Lesions in Basal Keratinocytes Attenuates Ultraviolet-Induced Skin Effects in Nucleotide Excision Repair Deficient Mice (2022) · cites this paper as [3]
Experimental — accuracy not yet measuredIn the citing paper
“However, it can act as a photosensitizer and can promote the formation of secondary photoproducts [1,7].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [7]
In the citing paper
“UV-A, on the other hand, is a much less deleterious damaging factor than UV-B because it is not so effectively absorbed by the DNA.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [7]
In the citing paper
“In summary defects in the DDR components may lead to malfunctioning of cell-cycle checkpoint and enhance the genomic instability of defective cells [7].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [7]
In the citing paper
“NER is a highly versatile and sophisticated DNA repair pathway that counteracts the deleterious effects of numerous structurally unrelated DNA lesions, including lesions that distort the DNA double helix, interfere in base pairing and block DNA duplication and transcription [34].”
From Sunlight damage to cellular DNA: focus on oxidatively generated lesions (2017) · cites this paper as [34]
In the citing paper
“As described previously, NER is one of the most versatile DNA repair systems for eliminating a variety of helix-distorting DNA lesions induced by UVR [47].”
From Ultraviolet Radiation‐Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging (2016) · cites this paper as [47]
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Self-check results appear here once an independent check has confirmed them.
Cited works that were retracted
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In the paper
“[224] has revealed that CSB is a prerequisite factor in vivo to assemble NER proteins while it is not essential to recruit TFIIH or NER complex in vitro.”
Cited work 10.1016/j.molcel.2006.06.029 · retracted 2021-12-16 · notice 10.1016/j.molcel.2021.11.021 · this paper published 2010-01
A note, not an issue: for example, a cited work that was retracted only after this paper was published, which its authors could not have known.
In the paper
“10.1016/j.molcel.2007.06.014”
Cited work 10.1016/j.molcel.2007.06.014 · retracted 2021-12-16 · notice 10.1016/j.molcel.2021.11.022 · this paper published 2010-01
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“If not repaired in a timely manner, these UV-induced photolesions can cause severe structural distortions in DNA and affect important cellular processes, including DNA replication and transcription.(3) miRNAs have been shown to regulate many biological processes such as embryonic development, cell differentiation, apo…”
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“These photoproducts (i.e., lesions) can cause DNA to make an unnatural conformation, arresting replication (Rastogi et al. 2010).”
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“, the photoproduct cyclobutan pyrimidine dimer (CPD), single-strand breaks (SSBs), and DSBs (32, 64, 65).”
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“Conversely, damage too severe to be repaired will cause the cell to go to apoptosis or acute necrosis [3], [23],”
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“UV light has been demonstrated to alter a cell’s proliferative capabilities by inducing DNA damage and prolonged UV exposure can result in cell death.(11,12) UV laser wavelengths are increasingly used in flow cytometry and cell sorting to excite not only DNA dyes such as Hoechst and DAPI but also a broad range of fluo…”
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“16,17 Consequently, there is an urgent need to develop targeted prevention and control policies that are informed by the regional distribution of disease burden, particularly focusing on areas where the burden has escalated in recent years.”
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Metadata
- Authors
- Rastogi, R. P., Richa, Kumar, A., Tyagi, M. B., & Sinha, R. P.
- Affiliations
- Banaras Hindu University (IN)
- Corresponding author
- Sinha, Rajeshwar P.
- Venue
- Journal of Nucleic Acids
- Publisher
- Wiley
- Published
- 2010-01
- Volume
- 2010
- Issue
- 1
- Pages
- 592980-592980
- ISSN
- 2090-0201 (ISSN-L)
- 2090-021X
- PMC
- PMC3010660
- OpenAlex
- W2026743476
- Semantic Scholar
- d11b9812b969c7d3d30c2829e21f6da372ae74ec
- Cited by
- 1,329
- References
- 366
- Citations by year
- 2026: 101 · 2025: 134 · 2024: 113 · 2023: 116 · 2022: 114 · 2021: 152 · 2020: 117 · 2019: 85 · 2018: 85 · 2017: 62 · 2016: 58 · 2015: 53 · 2014: 52 · 2013: 40 · 2012: 22
- FWCI
- 11.06
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Nucleic Acids (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- University Grants Commission
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- ultraviolet radiation, UV-B radiation, DNA damage, DNA repair, cyclobutane pyrimidine dimers, 6-4 photoproducts, DNA strand breaks, photoreactivation, base excision repair, nucleotide excision repair, DNA mismatch repair, homologous recombination, non-homologous end joining, SOS response, cell cycle checkpoints, apoptosis, genome stability
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-09-28, under version 3 of the claim definition (prompt extract-v3).
A second model labelled each claim on 2026-09-28 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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