CoChat
Sign Up
Cited by 1,339DNA Repair MechanismsDNA and Nucleic Acid ChemistryCarcinogens and Genotoxicity Assessment

Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair

Open access
Rastogi, Rajesh P., Richa, Kumar, Ashok, Tyagi, Madhu B., Sinha, Rajeshwar P.·2010·Journal of Nucleic Acids
DOI 10.4061/2010/592980PMC PMC3010660
Open this paper in CoChat — free accountOpen PDF

Abstract

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.

Integrity signals

Registry

Crossref · 10.4061/2010/592980

Cites

364 of 364 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

73 of 334 cited sources checked · 29 supported · 1 flagged · accuracy not yet measured

  • Premisecitation

    Bending DNA toward the minor groove reduces CPD formation.

    “Bending of DNA towards the minor groove reduces CPDs formation [52].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
  • Premisecitation

    trans-syn CPD causes greater distortion than cis-syn CPD through a kink or dislocation at the 5′ side of the dimer in double-stranded DNA.

    “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].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [77] source

      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)

      Experimental — accuracy not yet measured
  • Premisecitation

    Complementary base pairing strongly suppresses the photoreactivity of adjacent adenine bases in DNA.

    “Moreover, photoreactivity of adjoining adenine bases in DNA is strongly suppressed by the complementary base pairing [50, 72].”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [50]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [72] source
  • Premisecitation

    NMR and X-ray studies of cis-syn CPD with S-cyanoethyl phosphotriester show the two pyrimidine bases rotated by −29° base twist, compared with the right-handed 36° value in B-form DNA.

    “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].”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [78] source

      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)

      Experimental — accuracy not yet measured
    • cites [79] source
  • Premisecitation

    In the CPD/GG duplex, the two thymine residues of the CPD form wobble base pairs with opposite guanines, similar to the T6-G15 pair in the CPD/GA duplex.

    “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].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
  • May combine two claims. 97
  • Classified as probably not a substantial claim. 31

  • May combine two claims.

    Premisecitation

    BER and NER, but not photoreactivation, are active in proliferating cells of higher plants.

    “Recently, it has been reported that the mechanisms of BER and NER (but not photoreactivation) in higher plants are active in proliferating cells [172].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [172] source

      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.

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    UVR is a highly effective carcinogenic exogenous agent that interacts with DNA, alters genome integrity, and may affect normal life processes from prokaryotes to mammals.

    “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].”
    Quote in the paperSubstantial claim3 of 9 sources checked
    • cites [2]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [3]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [4] source
    • cites [5]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [6] source
    • cites [7] source
    • cites [8] source

      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)

      Experimental — accuracy not yet measured
    • cites [9] source

      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)

      Experimental — accuracy not yet measured
    • cites [10] source

      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)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    TATA-box binding protein promotes selective 6-4PP formation in the bent TATA box, while CPDs form preferentially at the TATA box edge and outside where DNA is not bent.

    “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].”
    Quote in the paperNot a substantial claim1 of 1 sources checked

  • May combine two claims.

    Premisecitation

    Solar UV radiation causes diverse biological effects, including changes to protein and DNA structure, chronic depression of physiological processes, and acute stress that reduces growth, cell division, pigment bleaching, N2 fixation, energy production, or photosynthesis.

    “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”
    Quote in the paperNot a substantial claim2 of 3 sources checked
    • cites [3]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [9] source

      Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured
    • cites [10] source

      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)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Among UVR groups, UV-B produces adverse effects on diverse habitats, although most extraterrestrial UV-B is absorbed by stratospheric ozone.

    “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].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [12] source

      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)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    UV-absorbing pigments produced by some organisms act as a first line of defense but cannot completely prevent UV radiation from reaching DNA in superficial tissue.

    “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].”
    Quote in the paperNot a substantial claim1 of 5 sources checked
    • cites [28]
    • cites [29] source
    • cites [30] source
    • cites [31] source

      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)

      Experimental — accuracy not yet measured
    • cites [32] source

  • May combine two claims.

    Premisecitation

    Endogenous free radicals generated during metabolism and exogenous factors such as UV or ionizing radiation interfere with genome integrity.

    “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.”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [34] source
    • cites [35] source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Su et al. reported a new photoproduct of 5-methylcytosine and adenine characterized by HPLC and mass spectrometry.

    “However, Su et al. [61] have reported a new photoproduct of 5-Methylcytosine and Adenine characterized by high-performance liquid chromatography and mass spectrometry.”
    Quote in the paperNot a substantial claim1 of 1 sources checked

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Rumora et al. examined thymine dimer-induced structural changes in the DNA duplex using small base-selective reactive chemical probes.

    “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.”
    Quote in the paperNot a substantial claim1 of 1 sources checked

  • May combine two claims.

    Premisecitation

    UV-induced CPDs and 6-4PPs have differential effects on DNA conformation and impair regulatory functions and dynamic processes.

    “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].”
    Quote in the paperSubstantial claim1 of 4 sources checked
    • cites [24] source
    • cites [26] source

      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)

      Experimental — accuracy not yet measured
    • cites [75] source
    • cites [76]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The existence of DNA repair mechanisms was independently observed by Kelner and Dulbecco.

    “the existence of repair mechanisms was observed by Kelner [154] and Dulbecco [155] independently.”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [154] source

      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)

      Experimental — accuracy not yet measured
    • cites [155] source

  • May combine two claims.

    Premisecitation

    Plants have acquired two main protective strategies against UVR: shielding by flavonoids and phenolic compounds, and DNA repair by photoreactivation.

    “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.”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [168] source

      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)

      Experimental — accuracy not yet measured
    • cites [169] source

  • May combine two claims.

    Premisecitation

    Deprotonated reduced FADH− is the catalytic cofactor in all known photolyases and transfers an electron to the CPD, splitting the cyclobutane ring into two monomeric bases.

    “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]”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [157] source
    • cites [167] source

  • May combine two claims.

    Premisecitation

    CSA is a 44 kDa WD repeat protein with structural and regulatory roles, and CSB is a 168 kDa SWI/SNF protein with DNA-stimulated ATPase activity.

    “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].”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites [217] source
    • cites [218] source
    • cites [219] source

  • May combine two claims.

    Premisecitation

    The hHR23B-XPC complex, or XPC alone, binds UV-induced single-stranded and double-stranded DNA with similar high affinity, prefers DNA containing various lesions, and can bind small bubble structures with or without a lesion.

    “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].”
    Quote in the paperNot a substantial claim3 of 3 sources checked
    • cites [230] source

      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)

      Experimental — accuracy not yet measured
    • cites [259] source

      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)

      Experimental — accuracy not yet measured
    • cites [260] source

  • May combine two claims.

    Premisecitation

    hHR23B-XPC is required for both dual incision and open complex formation in global genome nucleotide excision repair.

    “hHR23B-XPC is absolutely required for dual incision as well as for open complex formation during GG-NER [243, 261].”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [243] source

      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)

      Experimental — accuracy not yet measured
    • cites [261] source

  • May combine two claims.

    Premisecitation

    XPA and RPA can be recruited to DNA lesions without XPG, and XPG can also join damage sites without XPA.

    “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].”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [238] source
    • cites [239] source

      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)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    hHR23A and hHR23B each carry a ubiquitin-like domain at their amino terminus.

    “Both hHR23A and -B harbor a ubiquitin-like moiety at their amino terminus [230].”
    Quote in the paperNot a substantial claim1 of 1 sources checked

  • May combine two claims.

    Interpretationcitation

    Transcription-coupled repair is carried out by RNA polymerase II with CSA and CSB, whereas global genome repair is initiated by hHR23B-XPC, which senses and binds lesions, distorts DNA locally, and recruits other NER factors.

    “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].”
    Quote in the paperNot a substantial claim1 of 1 sources checked

  • May combine two claims.

    Premisecitation

    The plant NER pathway is homologous to mammalian and fungal NER and is unrelated to the bacterial system.

    “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].”
    Quote in the paperNot a substantial claim1 of 4 sources checked
    • cites [204] source
    • cites [271] source

      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)

      Experimental — accuracy not yet measured
    • cites [272]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites [273]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation

    6-4PPs are removed much faster from the genome than CPDs, possibly because of differences in affinity of the damage sensor hHR23B-XPC.

    “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.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [211] source

      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)

      Experimental — accuracy not yet measured
    • The authors state this as an assumption: XPC preferentially binds single-stranded DNA in the non-damaged strand opposite a lesion.

  • May combine two claims.

    Premisecitation

    XPC is the only XP factor not essential for TCR and is restricted to GGR.

    “XPC is the sole XP factor not essential for TCR and is restricted to GGR [211].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [211] source

      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)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Rad51 is the central HR protein, binds exposed single-stranded tails to form a nucleoprotein filament, and this early step is promoted by the Rad55/Rad57 heterodimer by overcoming inhibition by RPA.

    “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].”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites [298] source

      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)

      Experimental — accuracy not yet measured
    • cites [299] source
    • cites [300]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation

    The Ku complex, a Ku70/Ku80 heterodimer, is a major end-binding factor in mammalian cells and has end-bridging activity.

    “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].”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [308] source
    • cites [309] source

  • May combine two claims.

    Premisecitation

    Eukaryotic RAD51 proteins play a significant role in HR and maintain genome integrity in both mitotic and meiotic cell cycles.

    “The eukaryotic RAD51s play a significant role in HR, maintaining genome integrity in both mitotic as well as meiotic cell cycle [288, 289].”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [288] source
    • cites [289] source

      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)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Genetic and biochemical evidence suggests that MRX acts as the end-bridging factor in yeast NHEJ because DNA-PKcs is absent in yeast.

    “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].”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [319] source

      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)

      Experimental — accuracy not yet measured
    • cites [320]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation

    A plant homologue of the human NER endonuclease ERCC1 has been cloned from Lilium longiflorum and has a similar role in plant DNA repair.

    “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].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [279] source

      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)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    The SOS repair system is initiated by interaction between RecA and the LexA repressor, which represses SOS genes by binding their promoters.

    “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).”
    Quote in the paperNot a substantial claim1 of 1 sources checked

  • May combine two claims.

    Premisecitation

    recA encodes a DNA-dependent ATPase that binds single-stranded DNA and promotes strand invasion and exchange between homologous DNA molecules.

    “The recA gene encodes a DNA-dependent ATPase that binds to ssDNA and promotes strand invasion and exchange between homologous DNA molecules [285].”
    Quote in the paperNot a substantial claim1 of 1 sources checked

  • May combine two claims.

    Premisecitation

    When repair mechanisms fail, cellular senescence, oncogenesis, or apoptosis may result.

    “When the repair mechanisms are unsuccessful, it may cause cellular senescence (permanent cell cycle arrest), oncogenesis or apoptosis [354].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [354] source

      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)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    The genes imuA and imuB induce SOS mutagenesis in Caulobacter crescentus but are absent in E. coli.

    “Recently, the genes imuA and imuB have been described that induce SOS mutagenesis in Caulobacter crescentus, but absent in E. coli [332].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [332] source

      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)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    A G2-phase DNA damage response causes claspin-dependent Chk1/2 activation and SCFβTrcP-mediated degradation of Cdc25A, arresting multiple cell-cycle transitions including the G2 checkpoint.

    “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].”
    Quote in the paperNot a substantial claim3 of 4 sources checked
    • cites [341] source

      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)

      Experimental — accuracy not yet measured
    • cites [342] source

      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)

      Experimental — accuracy not yet measured
    • cites [343] source
    • cites [344] source

      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)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Translesion synthesis past a CPD is facilitated by polymerase η, which inserts adenines opposite both bases of a T∧T CPD, whereas a 6-4TT lesion may lead to insertion of G.

    “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.”
    Quote in the paperNot a substantial claim1 of 1 sources checked

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    DNA polymerase IV (dinB) is also involved in translesion synthesis in E. coli.

    “Interestingly, it has been found that DNA polymerase IV (dinB) is also involved in translesion synthesis in E. coli [331].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [331] source

      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)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.

    Interpretationnone given

    Double-strand break repair by homologous recombination and nonhomologous end joining, SOS response, cell-cycle checkpoints, and apoptosis operate in various organisms and require specific gene products.

    “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.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisenone given

    Hydrolytic deamination converts one base to another; cytosine deamination yields uracil, and adenine deamination yields hypoxanthine at much lower frequency.

    “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.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    The spore photoproduct forms in UV-irradiated bacterial spores by addition of a methyl group from one thymine to C5 of an adjacent thymine; it is not significant in most cellular environments because it requires anhydrous conditions.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [49] source

  • May combine two claims.

    Premisecitation

    6-4PPs convert to Dewar valence isomers upon UV-B or UV-A exposure and can revert to 6-4PPs upon short-wavelength UV.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [45] source

  • May combine two claims.

    Premisenone given

    UV-B has less than 1% of total solar energy but is highly active and causes chemical modification of DNA by forming dimers.

    “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.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Enzymes such as SOD, CAT, and POD and scavengers such as vitamins C, B, and E, cysteine, and glutathione play an additional defensive role against UV radiation.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [33] source

  • May combine two claims.

    Premisecitation

    CPDs and 6-4PPs account for about 75% and 25% of total UV-mediated DNA damage products, respectively, but their ratio depends on the adjacent bases involved.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [22] source
    • cites [54] source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Ozone depletion and increased UV exposure are predicted to continue through most of this century.

    “Moreover, ozone depletion followed by increased UV exposure has been predicted to continue throughout most of this century [11].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [11] source

  • May combine two claims.

    Premisecitation

    The main photoproducts are cis-syn CPD lesions, while trans-syn CPD lesions form in much smaller amounts.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [47] source

  • May combine two claims.

    Premisereasoning

    Depurination and depyrimidination remove purine or pyrimidine bases, leaving deoxyribose sugar and potentially causing DNA backbone breakage.

    “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.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    The heterogeneous distribution of UV-induced photolesions depends on sequences that facilitate DNA bending and on chromatin modulation through specific protein binding.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [55] source

  • May combine two claims.

    Premisecitation

    CPDs form a four-member ring involving C5 and C6 of neighboring bases, while 6-4PPs form a noncyclic bond between C6 of the 5′ end and C4 of the 3′ end via oxetane or azetidine intermediates.

    “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”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [5] source
    • cites [44] source

  • May combine two claims.

    Premisecitation

    DNA damage can result in misincorporation of bases during replication, hydrolytic damage, oxidative damage, and alkylating agent-induced modified bases.

    “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”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [36] source
    • cites [37] source
    • cites [38] source

  • May combine two claims.

    Premisecitation

    Cellular DNA is a major target of solar UV radiation; it absorbs UV-B and causes adverse effects in bacteria, cyanobacteria, phytoplankton, macroalgae, plants, animals, and humans.

    “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].”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [15] source
    • cites [16] source
    • cites [17]
    • cites [18] source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    At high concentrations, oxygen-free radicals or reactive oxygen species can damage cell structure, lipids, proteins, and DNA, causing oxidative stress implicated in several human diseases.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [40] source

  • May combine two claims.

    Premisecitation

    CPDs form in higher amounts by cycloaddition between two pyrimidine bases in single-stranded DNA and at flexible ends of poly(dA)-(dT) tracts, but not at their rigid center.

    “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].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [47] source
    • cites [50] source
    • cites [51] source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisereasoning

    UV-C is quantitatively absorbed by atmospheric oxygen and ozone and therefore has little harmful effect on biota.

    “UV-C radiation is quantitatively absorbed by oxygen and ozone in the Earth's atmosphere, hence does not show much harmful effects on biota.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    UV-B severely affects survival, fecundity, and sex ratio in several intertidal copepods.

    “It has been documented that UV-B severely affects survival, fecundity, and sex-ratio in several intertidal copepods [14].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [14] source

  • May combine two claims.

    Premisecitation

    In double-stranded B-DNA, only syn isomers can be generated, and the cis isomer is strongly preferred over the trans isomer.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [42] source

  • May combine two claims.

    Premisecitation

    Adenine photodimerization involves cycloaddition of the N7-C8 double bond of the 5′-A across C6 and C5 of the 3′-A and generates a very unstable azetidine intermediate.

    “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.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [65] source
    • cites [69] source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Little information exists about cytosine hydrate formation in UV-irradiated DNA because the photoproduct is unstable.

    “There is little information concerning the formation of cytosine hydrates in UV-irradiated DNA due to instability of the resulting photoproduct [63].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [63] source

  • May combine two claims.

    Interpretationcitation

    UV-induced DNA lesions such as CPDs, 6-4PPs, abasic sites, strand breaks, and oxidative products are predominant and persistent; if unrepaired they can cause severe structural distortions, affect replication and transcription, compromise cellular viability, and lead to mutagenesis, tumorigenesis, and cell death.

    “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”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [30] source
    • cites [36] source

  • May combine two claims.

    Premisecitation

    Dipyrimidine photoproducts are the preferential outcome of UV-B radiation, but UV-induced modifications of purine bases also have biological importance.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [64] source

  • May combine two claims.

    Premisecitation

    UV-B-induced ROS and DNA lesions (CPDs and 6-4PPs) may cause primary and secondary breaks, respectively.

    “UV-B-induced ROS [89] as well as DNA lesions (CPDs and 6-4PPs) may cause primary as well as secondary breaks, respectively.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [89] source

  • May combine two claims.

    Premisecitation

    Adenine-containing photoproducts (A-T) occur at very low levels (1 × 10−5 in native DNA) but may contribute to UV biological effects because the A-T adduct is mutagenic.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [67] source
    • cites [68] source

  • May combine two claims.

    Premisecitation

    DNA photolyases are monomeric flavin-dependent repair enzymes of 45-66 kDa with 420-616 amino acid residues and two known cofactors, one catalytic and one light-harvesting.

    “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.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [158] source

  • May combine two claims.

    Premisenone given

    Photoreactivation is carried out by photolyase, an enzyme that is well conserved and present across the three domains of life.

    “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).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    6-4 photolyases have been identified in organisms including Drosophila, silkworm, Xenopus laevis, and rattlesnakes.

    “6-4 photolyases have been identified in certain organisms like Drosophila, silkworm, Xenopus laevis, and rattle snakes [22].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [22] source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    CPD photolyases have been reported in archaea, bacteria, fungi, viruses, plants, invertebrates, and many vertebrates including aplacental mammals.

    “CPD photolyases have been reported in diverse groups such as archaea, bacteria, fungi, virus, plants, invertebrates, and many vertebrates including aplacental mammals (Table 2).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    About 240 kJ/mol of energy is captured upon absorption, and about 125 kJ/mol is consumed during the initial electron transfer from excited FADH to CPD lesions.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [177] source

  • May combine two claims.

    Interpretationcitation

    UV-induced replication arrest in xeroderma pigmentosum variant, followed by accumulation of Mre11/Rad50/Nbs1 complex and phosphorylated histone H2AX in large nuclear foci at stalled replication forks, suggests that UV damage leads to DSB formation during replication arrest.

    “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].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [90] source
    • cites [95] source
    • The authors state this as an assumption: Initial UV photoproducts are converted into DNA double-strand breaks during replication through collapse of replication forks.

  • May combine two claims.

    Premisecitation

    Photolyase binds specifically to CPDs or 6-4PPs and directly monomerizes the cyclobutane ring of the pyrimidine dimer using visible or blue light, protecting the genome from UVR damage.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [157] source
    • cites [158] source

  • May combine two claims.

    Premisecitation

    Studies on Arabidopsis seedlings, rice, and alfalfa indicate that photoreactivation greatly increases dimer removal, while without blue light dimers are slowly eliminated and 6-4PPs are generally repaired more quickly than CPDs.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [173] source
    • cites [174] source

  • May combine two claims.

    Premisecitation

    A human photolyase has been identified that is homologous to the plant blue-light receptor Cry gene and shares about 40% sequence identity with Drosophila 6-4 photolyase.

    “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”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [164] source

  • May combine two claims.

    Interpretationreasoning

    UV radiation does not directly produce DNA DSBs but rather produces pyrimidine dimers and other photoproducts that lead to replication arrest and DSBs.

    “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.”
    Quote in the paperSubstantial claim
    • The authors state this as an assumption: Initial UV photoproducts are converted into DNA double-strand breaks during replication through collapse of replication forks.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    MacFarlane and Stanley suggested that photolyase remains in a semiquinonid state after repairing the CPD lesion.

    “MacFarlane and Stanley [178] have suggested that photolyase enzyme is indeed left in the semiquinonid state after accomplishment of repair of the CPD lesion.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [178] source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Almeida and Sobol proposed a unified model of short-patch and long-patch BER.

    “Recently, Almeida and Sobol [184] have proposed a unified model of SP-BER and LP-BER.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [184] source

  • May combine two claims.

    Premisecitation

    Eukaryotic NER uses a biochemical strategy similar to that of prokaryotes but differs widely in the nature and number of proteins used.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [210] source

  • May combine two claims.

    Premisecitation

    APE-1 with phosphodiesterase removes the AP site by breaking the DNA strand 5′ or 3′ to it, after which a repair DNA polymerase fills the gap and DNA ligase joins the strand.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [182] source
    • cites [191] source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    NER was first described in E. coli, where about six proteins-UvrA, B, and C (the ABC complex with excinuclease activity), UvrD (helicase II), DNA polymerase I, and DNA ligase-are recruited to complete repair.

    “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].”
    Quote in the paperNot a substantial claim0 of 4 sources checked
    • cites [212] source
    • cites [213] source
    • cites [214] source
    • cites [215] source

  • May combine two claims.

    Premisecitation

    Short-patch BER removes DNA with a one-nucleotide lesion, while long-patch BER repairs lesions of two or more nucleotides.

    “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).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [195] source
    • 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.

  • May combine two claims.

    Premisecitation

    Fen1 displaces the resulting DNA flap, leaving a nick that DNA ligase I ligates.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [200] source
    • cites [201] source

  • May combine two claims.

    Premisecitation

    AP sites form in Zea mays seeds during early germination, attributed to DNA glycosylases acting on lesions accumulated during seed storage, implying BER in this species.

    “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.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [207] source

  • May combine two claims.

    Premisecitation

    Long-patch BER involves PCNA with DNA polymerase δ/ε or β, which extends and fills the gap by inserting 2-13 nucleotides.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [184] source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    RNA polymerase II backs up some nucleotides upon encountering a lesion to facilitate access of the repair machinery to the lesion site.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [220] source
    • cites [221] source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    CSB protein ubiquitinates the stalled elongating RNA polymerase II complex at the lesion and enhances assembly of repair factors.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [222] source

  • May combine two claims.

    Premisecitation

    Fousteri et al. revealed that CSB is a prerequisite factor in vivo for assembling NER proteins, while it is not essential for recruiting TFIIH or the NER complex in vitro.

    “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.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [224] source

  • May combine two claims.

    Premisecitation

    TFIIH normally functions in RNA polymerase II transcription initiation, but after DNA damage it can also act in cell-cycle regulation and in both global genome and transcription-coupled NER.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [228] source
    • cites [235] source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    In mammalian cells, hHR23B is more abundant than XPC.

    “In mammalian cells, the quantity of hHR23B is higher than the XPC [255]”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [255] source

  • May combine two claims.

    Premisecitation

    The hHR23B-XPC complex binds directly to damaged DNA and changes the DNA conformation near the lesion.

    “Sugasawa et al. [226] showed that hHR23B-XPC attaches directly to DNA damage and alters the DNA conformation around the lesion.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [226] source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    TFIIH is a ten-subunit complex made of a core complex and a CAK subunit.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [236] source

  • May combine two claims.

    Premisecitation

    XPA and heterotrimeric RPA are recruited to verify DNA damage and to form a more stable preincision complex.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [185] source

  • May combine two claims.

    Premisecitation

    XPD helicase activity is not needed for in vitro transcription, but XPD appears to have an architectural role linking the TFIIH core to the CAK subunit.

    “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].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [262] source
    • cites [228] source
    • cites [236] source

  • May combine two claims.

    Premisecitation

    Ligase III with XRCC1 seals DNA nicks, while ligase I has a minor role in actively replicating cells but not in quiescent cells.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [268] source

  • May combine two claims.

    Premisecitation

    Dark repair of UV-induced damage is a significant DNA repair mechanism in plants and can excise dimers, especially 6-4PPs.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [30] source
    • cites [270] source

  • May combine two claims.

    Premisecitation

    The DDB complex is recruited first to a CPD lesion before the XPC complex on little distorted DNA, while for large distortion caused by 6-4PPs, direct recognition by XPC is also possible.

    “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”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [216] source
    • cites [253] source

  • May combine two claims.

    Premisecitation

    XPC and UV-DDB assist efficient recognition of UV-induced photolesions, and both factors are ubiquitylated.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [250] source
    • cites [253] source

  • May combine two claims.

    Premisecitation

    Lesions causing little distortion can be recognized by the DDB complex, which is part of an E3 ubiquitin ligase that poly-ubiquitinates XPC and XPE.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [216] source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    A UV-specific endonuclease with activity resembling UvrABC nuclease has been partially characterized from spinach.

    “A UV-specific endonuclease resembling UvrABC nuclease in activity was partially characterized from spinach [206].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [206] source

  • May combine two claims.

    Premisecitation

    XPG, a FEN-1 family structure-specific endonuclease, performs the 3′ incision in NER and also stabilizes the open DNA bubble to allow the 5′ incision by ERCC1-XPF.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [264] source
    • cites [265] source

  • May combine two claims.

    Premisecitation

    Recombinational repair is a significant UV-tolerance mechanism in plants, where UV-induced chromosomal rearrangements including homologous intrachromosomal recombination events have been found.

    “Recombinational repair is a significant UV-tolerance mechanism in plants where UV-induced chromosomal rearrangements including homologous intrachromosomal recombination events have been found [296].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [296] source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisenone given

    In E. coli, Holliday junctions are resolved by the RuvABC resolvasome, but in eukaryotic cells how Holliday junctions are resolved to produce crossovers is unknown.

    “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.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Accumulation of massive DNA lesions under specific physiological responses may trigger the SOS repair system, which is well described in E. coli and involves more than 40 genes.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [324] source
    • cites [325] source

  • May combine two claims.

    Premisecitation

    When HR is inactivated, NHEJ becomes operative for DSB repair; NHEJ involves a multi-protein complex and occurs in organisms from some prokaryotes to mammals.

    “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.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [303] source

  • May combine two claims.

    Premisecitation

    Most RAD52 epistasis group genes have highly conserved homologues among eukaryotes, including humans, which highlights their importance for cell survival.

    “Homologues of most of the genes are highly conserved among all eukaryotes including human [282, 283] highlighting these genes for cell survival.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [282] source
    • cites [283] source

  • May combine two claims.

    Premisereasoning

    RecA proteolytic activity inactivates LexA and induces all genes associated with LexA.

    “The proteolytic activity of RecA protein inactivates the LexA repressor and induces all the genes to which LexA is associated.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Mutation of at least one repair protein, BRCA1, may lead to hereditary breast cancer.

    “For instance, mutation of at least one of these repair proteins, called BRCA1 may lead to hereditary breast cancer [280].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [280] source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The E. coli recA gene and its eukaryotic RAD51 homologues are the best-characterized recombination genes.

    “Among all, E. coli recA gene and its eukaryotic homologs RAD51s are the best recombination genes [284].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [284] source

  • May combine two claims.

    Premisereasoning

    The Rad51 nucleoprotein filament with other repair proteins searches the genome for an intact sister-chromatid copy, forms heteroduplex joint molecules or a D-loop, matures into Holliday junctions, and these junctions are resolved to give crossover products.

    “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).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    After joint molecule formation, DNA polymerases extend the incoming strand and branch migration occurs, restoring the genetic information.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [283] source
    • cites [302] source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Yeasts S. cerevisiae and S. pombe have four RAD51-like genes, while vertebrates and plants have seven RAD51-like genes.

    “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].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [286] source
    • cites [287] source
    • cites [288] source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Rad51 protein is 59% identical among S. cerevisiae, human, and mouse and 30% identical to bacterial RecA, while yeast and human Rad52 proteins are 60% identical.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [290] source
    • cites [291] source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    As in mammals, plant breaks are suggested to be repaired by nonhomologous recombination much more often than by HR.

    “It has been suggested that as in mammals, breaks are repaired by nonhomologous recombination far more frequently than via HR [202, 323].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [202] source
    • cites [323] source

  • May combine two claims.

    Premisereasoning

    HR repairs DSBs without error because it requires extensive sequence homology between damaged and template strands, whereas NHEJ is an error-prone alternative that joins broken chromosomal ends without requiring sequence homology.

    “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.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    XLF/Cernunnos, a protein homologous to Xrcc4, has been identified and co-associates with the DNA ligase IV/Xrcc4 complex.

    “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].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [313] source
    • cites [314] source
    • cites [315] source

  • May combine two claims.

    Premisecitation

    β-TrcP links WEE1 and claspin to the SCF ubiquitin ligase complex, and SCFβTrcP triggers checkpoint initiation and recovery through Plk1-mediated phosphorylation of claspin and WEE1.

    “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”
    Quote in the paperNot a substantial claim0 of 5 sources checked
    • cites [346] source
    • cites [347] source
    • cites [348] source
    • cites [349] source
    • cites [350] source

  • May combine two claims.

    Premisecitation

    Active cyclinB-Cdk1 promotes the G2/M transition; its inactivation by DNA damage blocks the G2 cell cycle, and this arrest appears partly independent of p53/p21, unlike the G1/S checkpoint.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [183] source

  • May combine two claims.

    Premisereasoning

    ATM and ATR activation phosphorylates Chk2 and Chk1, respectively, which transmit the DNA damage signal to Cdc25(A-C) proteins.

    “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).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    ATM and DNA-PK are activated by DSBs, whereas ATR is activated by single-stranded DNA regions.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [337] source
    • cites [338] source

  • May combine two claims.

    Premisecitation

    The SOS response is induced by a damage signal but is highly mutagenic because it uses error-prone DNA polymerase V and DNA polymerase IV in E. coli.

    “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.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [329] source
    • cites [330] source

  • May combine two claims.

    Premisecitation

    Majchrzak et al. found that SOS response genes destabilized trinucleotide repeat tracts and altered plasmid superhelical density in E. coli.

    “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.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [324] source
115 of 115

  • 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]”
9 of 9

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?

  • 6-4PP lesions cause a more pronounced distortion on the DNA molecule (44° bend) than CPDs (9° bend).

    “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]

    Section 5 (page unavailable) says 6-4PPs distort the DNA helix more than CPDs and reports a 44° bend for 6-4PPs. It does not give a 9° bend for CPDs; the other bending angle it reports, 21°, is for Dewar lesions. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • UV-A can act as a photosensitizer and promote formation of secondary photoproducts.

    “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]

  • UV-A is a much less deleterious DNA-damaging factor than UV-B because it is not so effectively absorbed by DNA.

    “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]

  • Defects in DDR components may lead to malfunctioning of cell-cycle checkpoint and enhance genomic instability of defective cells.

    “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]

  • NER is a highly versatile DNA repair pathway that counteracts 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.

    “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]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Self-check results appear here once an independent check has confirmed them.

Cited works that were retracted

Works this paper cites that were later retracted, from the retraction notices publishers deposit. Major when the notice came out before this paper was published.

  • Cites a retracted work: 10.1016/j.molcel.2006.06.029

    Info

    The cited work was retracted on 2021-12-16 (notice 10.1016/j.molcel.2021.11.021), not before this paper was published (2010-01).

    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

  • Cites a retracted work: 10.1016/j.molcel.2007.06.014

    Info

    The cited work was retracted on 2021-12-16 (notice 10.1016/j.molcel.2021.11.022), not before this paper was published (2010-01).

    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

2 of 2

Cites

2 retracted

Flagged first, then by citations

2 of the 366 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. Sinha R. P., 2008, Life of wetland cyanobacteria under enhancing solar UV-B radiation, Proceedings of the National Academy of Sciences, India B, 78, 53
  2. Taylor R., 1996, Nucleotide sequence of an Arabidopsis cDNA At-phrII encoding a protein with high homology to the class II CPD photolyases present in higher eukaryotes, Plant Physiology, 112, 862

Cited by

Sorted by citations

Related

Authors
Rastogi, R. P., Richa, Kumar, A., Tyagi, M. B., & Sinha, R. P.
Affiliations
Banaras Hindu University (IN)
Corresponding author
Sinha, Rajeshwar P.
ORCID
Venue
Journal of Nucleic Acids
Publisher
Wiley
Published
2010-01
Volume
2010
Issue
1
Pages
592980-592980
ISSN
  • 2090-0201 (ISSN-L)
  • 2090-021X
DOI
10.4061/2010/592980
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
Licence
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.

Claims read under definition version 3 (extract-v3) on 2026-09-28.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-09-28.

Cited sources are checked by 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 ›

Are you an author, or do you see a problem with this page? Request a review