The Human LINE-1 Retrotransposon Creates DNA Double-strand Breaks
Open accessAbstract
Long interspersed element-1 (L1) is an autonomous retroelement that is active in the human genome. The proposed mechanism of insertion for L1 suggests that cleavage of both strands of genomic DNA is required. We demonstrate that L1 expression leads to a high level of double-strand break (DSB) formation in DNA using immunolocalization of gamma-H2AX foci and the COMET assay. Similar to its role in mediating DSB repair in response to radiation, ATM is required for L1-induced gamma-H2AX foci and for L1 retrotransposition. This is the first characterization of a DNA repair response from expression of a non-long terminal repeat (non-LTR) retrotransposon in mammalian cells as well as the first demonstration that a host DNA repair gene is required for successful integration. Notably, the number of L1-induced DSBs is greater than the predicted numbers of successful insertions, suggesting a significant degree of inefficiency during the integration process. This result suggests that the endonuclease activity of endogenously expressed L1 elements could contribute to DSB formation in germ-line and somatic tissues.
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AI snapshot
Written from the paper’s full text.
TL;DR
L1 expression induces DNA double-strand breaks (DSBs) in mammalian cells, detected by γ-H2AX foci and neutral COMET, and this requires L1 endonuclease activity. ATM is required for L1-induced γ-H2AX foci and for L1 retrotransposition.
Key findings
- L1.3 transfection in HeLa produced γ-H2AX foci in 60–70% of cells, with 20–200 foci per focus-positive cell (mean 68), similar to 6 Gy ionizing radiation (mean 86); an endonuclease mutant (EN–) essentially abolished foci.
- Neutral COMET showed pronounced tail moments at 24 h after L1.3, with no tails at 48 h; L1-induced foci were largely repaired by 48 h.
- L1.3 cotransfection reduced neoR colony yield by 60%; EN– showed no significant toxicity, while RT– showed toxicity similar to wild-type L1.3. L1.3 reduced the mitotic index, whereas empty vector or EN– did not induce checkpoint responses.
- In ATM+ YZ-5 cells, synL1_optORF1_neo produced 62±6 and 24±10 L1 colonies; in ATM– EBS-7 cells, 0 colonies, while neoR plasmid controls were 207±38, 133±10, 115±12, and 91±4.7. L1-induced DSBs exceed insertions; the paper estimates conservatively tenfold more DSBs than insertions, with 100-fold within reason.
Methods
- Transient transfections of L1.3, L1 EN–, L1 RT–, ORF2, and synL1_optORF1_neo into HeLa, mouse 3T3, MCF7, and isogenic YZ-5 (ATM+) / EBS-7 (ATM–) cells.
- DSBs assessed by anti-γ-H2AX immunofluorescence and neutral single-cell gel electrophoresis (COMET); retrotransposition by G418 colony formation; toxicity by cotransfected neoR colony yield; cell-cycle by mitotic index; apoptosis by annexin V FACS/TUNEL.
- Main comparisons were between wild-type L1 and endonuclease/reverse transcriptase mutants, empty vector, and ATM+ versus ATM– cells; colony counts reported with SD.
Limitations
- Stated: the mechanism of second-strand cleavage is unresolved; whether ORF2 makes both breaks, uses another enzyme, or homes to existing nicks remains to be determined.
- Stated: poor understanding of L1 RNA/protein nuclear transport; overexpression may skew the DSB:insertion ratio by titrating repair factors or producing ORF2 activity unrelated to integration; a quantitative assay of L1 integration intermediates without selectable cassettes is needed.
- Stated/evident: fixed-cell γ-H2AX counts underestimate total breaks (the paper says slightly underestimate expected by about two- to threefold) and do not integrate frequency over time; most experiments use transformed cell lines and overexpressed L1, so relevance to endogenous L1 in normal tissues is not directly established (evident).
Model-written summary. Check it against the paper before relying on it.
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Cites
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Claims the paper makes
0 of 10 cited sources checked · 0 supported · 0 flagged
- Findingown data§ Abstract
ATM is required for L1 retrotransposition.
“Similar to its role in mediating DSB repair in response to radiation, ATM is required for L1-induced γ-H2AX foci and for L1 retrotransposition.”
- Also stated in: § Results · plain
“As shown in Table 1, synL1_optORF1_neo produced colonies efficiently in ATM+ cells. No colonies were detected in ATM– cells.”
Quote in the paperSubstantial claim - Also stated in: § Results · plain
- Findingown data§ Abstract
ATM is required for L1-induced γ-H2AX foci.
“Similar to its role in mediating DSB repair in response to radiation, ATM is required for L1-induced γ-H2AX foci and for L1 retrotransposition.”
- Also stated in: § Results · plain
“L1.3 expression induced γ-H2AX foci in ATMC but not in ATMK cells with exposure times normalized to observation of IR-induced foci in ATM+ (Figure 5).”
Quote in the paperSubstantial claim - Also stated in: § Results · plain
- Findingreasoning§ Abstract
The number of L1-induced DSBs is greater than the predicted number of successful insertions, conservatively estimated at tenfold more and possibly 100-fold more.
“Notably, the number of L1-induced DSBs is greater than the predicted numbers of successful insertions, suggesting a significant degree of inefficiency during the integration process.”
- Also stated in: § Results · hedged
“Therefore, it is conservative to estimate that tenfold more L1-induced DSBs are produced than insertions, although a 100-fold difference is within reason (our γ-H2AX counts slightly underestimate the expected by about twoto threefold39,40).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [39] Rothkamm K, Lobrich M. Evidence for a lack of DNA double-strand break repair in human cells exposed to very low x-ray doses. Proc. Natl Acad. Sci. USA. 2003;100:5057–5062. doi: 10.1073/pnas.0830918100. [DOI] [PMC free article] [PubMed] [Google Scholar] source
Not checked in the free run.
- cites [40] Sedelnikova OA, Rogakou EP, Panyutin IG, Bonner WM. Quantitative detection of (125)IdU-induced DNA double-strand breaks with gamma-H2AX antibody. Radiat. Res. 2002;158:486–492. doi: 10.1667/0033-7587(2002)158[0486:qdoiid]2.0.co;2. [DOI] [PubMed] [Google Scholar] d'Adda d. F., Reaper PM, Clay-Farrace L, Fiegler H, Carr P, Von Zglinicki T, et al. A DNA damage checkpoint response in telomere-initiated senescence. Nature. 2003;426:194–198. doi: 10.1038/nature02118. [DOI] [PubMed] [Google Scholar] source
Not checked in the free run.
- Also stated in: § Results · hedged
- Findingown data§ Results
L1-induced γ-H2AX foci are largely repaired by 48 h post transfection.
“The L1-induced foci are largely repaired by 48 h post transfection, as evidenced by the decreasing percentage of cells with γ-H2AX foci and the decreasing number of γ-H2AX foci per cell (Figure 2(b)).”
Quote in the paperNot a substantial claim - Findingown data§ Results
Mutations in the endonuclease domain of L1 ORF2 result in essentially complete loss of γ-H2AX foci in HeLa cells.
“Mutations in the endonuclease domain of the L1 ORF2 resulted in essentially complete loss of the γ-H2AX foci in HeLa cells (Figure 2(a)), consistent with the inability of the endonuclease mutant of L1 to support retrotransposition.44”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [44] Moran JV, Holmes SE, Naas TP, DeBerardinis RJ, Boeke JD, Kazazian HH., Jr High frequency retrotransposition in cultured mammalian cells. Cell. 1996;87:917–927. doi: 10.1016/s0092-8674(00)81998-4. [DOI] [PubMed] [Google Scholar] source
Not checked in the free run.
- Findingown data§ Results
L1.3 RT- produces fewer γ-H2AX foci than wild-type L1.3.
“L1.3 RT– produced fewer foci than observed with wild-type L1.3, suggesting that high levels of focus formation may depend on the presence of the first L1 cDNA strand.”
Quote in the paperSubstantial claim - Findingown data§ Results
MCF7 cells show the same induction of γ-H2AX foci following wild-type L1 transfections.
“The observation that MCF7 cells show the same induction of γ-H2AX foci following wild-type L1 transfections suggests that the response is not likely due to apoptosis (Figure 2(d)).”
Quote in the paperSubstantial claim - Findingown data§ Results
Transient inhibition of ATM with kinase inhibitors or a dominant negative plasmid in HeLa cells demonstrates involvement of ATM in promoting retrotransposition.
“Transient inhibition of ATM with kinase inhibitors or a dominant negative plasmid in HeLa cells (data not shown) also demonstrate the involvement of ATM in promoting retrotransposition.”
Quote in the paperSubstantial claim - Findingown data§ Results
L1.3 expression in mouse 3T3 cells produces high numbers of distinct γ-H2AX foci at 24 h post transfection.
“At 24 h post L1.3 transfection, 3T3 cells have high numbers of distinct foci as observed for HeLa cells (Figure 2(c)).”
Quote in the paperSubstantial claim - Findingown data§ Results
Over-expression of ORF2 alone results in only modest numbers of γ-H2AX foci 24 h post transfection.
“Over-expression of ORF2 alone resulted in the formation of only modest numbers of foci 24 h post transfection (Figure 2(c)).”
Quote in the paperSubstantial claim - Findingown data§ Results
Cotransfection with L1.3 reduces colony yield by 60% compared to vector in HeLa cells.
“Cotransfection with L1.3 reduced the colony yield by 60% compared to vector (Figure 4(a)).”
Quote in the paperSubstantial claim - Findingown data§ Results
L1.3 expression reduces the number of cells entering mitosis in HeLa cells.
“L1.3 expression reduced the number of cells entering mitosis, whereas neither empty vector nor EN– induced checkpoint responses in HeLa cells (Figure 4(b)).”
Quote in the paperSubstantial claim - Interpretationown data§ Discussion
Activation of H2AX and the disappearance of DSBs in a time-course suggests that L1 induces a DNA repair response.
“Activation of H2AX and the disappearance of DSBs in a time-course (Figures 2 and 3), suggests that L1 induces a DNA repair response.”
Quote in the paperSubstantial claim - Premisecitation§ Discussion
Computational analyses of de novo L1 integrations and genomic L1 integrations have shown that most integrations proceed through a microhomology process for priming L1 DNA synthesis.
“Computational analyses of de novo L1 integrations and genomic L1 integrations have shown that most integrations proceed through a microhomology process for priming L1 DNA synthesis.9”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9] Zingler N, Willhoeft U, Brose HP, Schoder V, Jahns T, Hanschmann KM, et al. Analysis of 5′ junctions of human LINE-1 and Alu retrotransposons suggests an alternative model for 5′-end attachment requiring microhomology-mediated end-joining. Genome Res. 2005;15:780–789. doi: 10.1101/gr.3421505. [DOI] [PMC free article] [PubMed] [Google Scholar] source
Not checked in the free run.
- Interpretationreasoning§ Discussion
Full levels of DSB activity per element likely require a largely intact ORF1 for both RNP formation/localization and interactions with the genome.
“Nonetheless, full levels of DSB activity per element are likely to still require a largely intact ORF1 for both RNP formation/ localization and interactions with the genome.”
Quote in the paperNot a substantial claim - Interpretationcitation§ Results
L1-induced DSBs appear to be less toxic than those from ionizing radiation.
“L1-induced DSBs appear to be less toxic than those from IR.58”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [58] Elkind MM. Repair processes in radiation biology. Radiat. Res. 1984;100:425–449. [PubMed] [Google Scholar] source
Not checked in the free run.
- Interpretationown data§ Discussion
This is the first evidence that the non-LTR class of retrotransposons depend on a cellular DNA repair enzyme for standard TPRT mobilization in eukaryotic cells.
“This is the first evidence that the non-LTR class of retrotransposons depend on a cellular DNA repair enzyme for standard TPRT mobilization in eukaryotic cells.”
Quote in the paperSubstantial claim - Interpretationreasoning§ Discussion
L1-induced DSBs could be a major contributor to chromosomal damage, including translocations, deletions and duplications.
“An important implication of L1-induced DSBs is that they could be a major contributor to chromosomal damage, including translocations, deletions and duplications.”
Quote in the paperSubstantial claim - Interpretationreasoning§ Discussion
The common requirement of different insertional elements on host DSB DNA repair proteins is likely due to the required modification of double-stranded DNA for insertion.
“The common requirement of these different insertional elements on host DSB DNA repair proteins is likely due to the required modification of double-stranded DNA for insertion.”
Quote in the paperNot a substantial claim - Interpretationown data§ Results
γ-H2AX foci likely represent true DSB formation directly induced by L1.
“Thus, γ-H2AX foci likely represent true DSB formation directly induced by L1.”
Quote in the paperSubstantial claim - Interpretationown data§ Results
The primary toxic lesion from L1 expression is dependent on the L1 endonuclease and not the synthesis of cDNA intermediates.
“Thus, the primary toxic lesion is dependent on the L1 endonuclease and not the synthesis of cDNA intermediates.”
Quote in the paperSubstantial claim - Interpretationown data§ Discussion
The presence of moderate levels of breaks when ORF2 is overexpressed suggests that the presence of ORF2 alone is insufficient for efficient DSB activity.
“The presence of moderate levels of breaks when ORF2 is overexpressed (Figure 2) suggests that the presence of ORF2 alone is insufficient for efficient DSB activity.”
Quote in the paperSubstantial claim - Interpretationreasoning§ Discussion
The genetic requirement for a DSB repair protein by L1 underscores the likelihood that DSBs represent a normal L1 integration intermediate.
“The genetic requirement for a DSB repair protein by L1 underscores the likelihood that DSBs represent a normal L1 integration intermediate.”
Quote in the paperSubstantial claim - Interpretationown data§ Results
High levels of L1-induced focus formation may depend on the presence of the first L1 cDNA strand.
“L1.3 RT– produced fewer foci than observed with wild-type L1.3, suggesting that high levels of focus formation may depend on the presence of the first L1 cDNA strand.”
Quote in the paperSubstantial claim - Interpretationown data§ Discussion
The requirement for endonuclease activity of ORF2 to produce L1-induced effects suggests a direct role for ORF2.
“The requirement for the endonuclease activity of ORF2 to produce these effects suggests a direct role for ORF2.”
Quote in the paperSubstantial claim - Interpretationown data§ Results
The reduction in neoR integration colonies in the absence of ATM is only twofold compared to ATM+, so the absolute defect in L1 retrotransposition is not likely due to a difference in colony formation or transfection competence between the two cell lines.
“Given that the reduction inneoR integration colonies in the absence of ATM was reduced only twofold compared to ATM+, the absolute defect in L1 retrotransposition is not likely to be due to a difference in colony formation or transfection competence between the two cell lines.”
Quote in the paperSubstantial claim - Interpretationown data§ Results
L1-induced γ-H2AX foci are not likely due to apoptosis.
“The observation that MCF7 cells show the same induction of γ-H2AX foci following wild-type L1 transfections suggests that the response is not likely due to apoptosis (Figure 2(d)).”
Quote in the paperSubstantial claim - Interpretationreasoning§ Discussion
Many elements with ORF1 or RT-inactivating mutations may still be capable of expressing a functional endonuclease that produces genomic DSBs.
“Many elements with ORF1 or RT-inactivating mutations may still be capable of expressing a functional endonuclease that produces genomic DSBs.”
Quote in the paperSubstantial claim - Interpretationown data§ Abstract
The endonuclease activity of endogenously expressed L1 elements could contribute to DSB formation in germ-line and somatic tissues.
“This result suggests that the endonuclease activity of endogenously expressed L1 elements could contribute to DSB formation in germ-line and somatic tissues.”
- Also stated in: § Discussion · hedged
“L1 may represent an important endogenous source of DSB-related genetic instability.”
Quote in the paperSubstantial claim- Rests on an assumption: The DSB formation observed from transfected L1 expression reflects the behavior of endogenously expressed L1 elements.
- Also stated in: § Discussion · hedged
- Interpretationown data§ Discussion
L1 may represent an important endogenous source of DSB-related genetic instability.
“L1 may represent an important endogenous source of DSB-related genetic instability.”
Quote in the paperSubstantial claim
- May combine two claims. 9
- Classified as probably not a substantial claim. 6
May combine two claims.
Findingown data§ AbstractL1 expression leads to a high level of double-strand break (DSB) formation in DNA, as shown by γ-H2AX foci and the COMET assay.
“We demonstrate that L1 expression leads to a high level of double-strand break (DSB) formation in DNA using immunolocalization of γ-H2AX foci and the COMET assay.”
- Also stated in: § Results · plain
“γ-H2AX foci were present in L1.3-transfected HeLa cells in high numbers and high focus intensity 24 h after transfection (Figure 2(a)).”
- Also stated in: § Results · plain
“Transfection with L1.3 produced pronounced tail-moments at 24 h post transfection in the majority of cells (Figure 3).”
Quote in the paperSubstantial claim- Also stated in: § Results · plain
May combine two claims.
Findingown data§ ResultsL1 EN- shows no significant toxicity, while L1.3 RT- shows toxicity levels similar to wild-type L1.3.
“L1 EN– showed no significant toxicity, while L1.3 RT– showed toxicity levels similar to that of the wild-type L1.3.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown data§ DiscussionAlthough most full-length L1 elements in the human genome are defective, the data suggest that more may be capable of causing genomic damage than the limited number capable of active retrotransposition.
“Although most full-length L1 elements in the human genome are defective, our data suggest that more may be capable of causing genomic damage than the limited number capable of active retro-transposition.78”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [78] Brouha B, Schustak J, Badge RM, Lutz-Prigge S, Farley AH, Moran JV, Kazazian HH., Jr Hot L1s account for the bulk of retrotransposition in the human population. Proc. Natl Acad. Sci. USA. 2003;100:5280–5285. doi: 10.1073/pnas.0831042100. [DOI] [PMC free article] [PubMed] [Google Scholar] source
Not checked in the free run.
May combine two claims.
Interpretationown data§ ResultsATM is specifically required for retrotransposition and not survival of cells after L1 expression.
“Notably, a modified toxicity assay shows no L1-induced toxicity in the ATM– cell line (data not shown), suggesting that ATM is specifically required for retrotransposition and not the survival of cells after L1 expression.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown data§ ResultsORF2 expression alone is sufficient for generating DSBs, but it is probably facilitated by the presence of ORF1.
“Thus, ORF2 expression alone is sufficient for generating DSBs, but it is probably facilitated by the presence of ORF1.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim.
Premisecitation§ IntroductionThe current model for non-LTR element insertion is target-primed reverse transcription (TPRT), based on in vitro analysis of R2Bm.
“On the basis of in vitro analysis of the R2 element from the silkworm Bombyx mori (R2Bm), the current model for non-long terminal repeat (non-LTR) element insertion is target-primed reverse transcription (TPRT) (Figure 1).6,7”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [6] Luan DD, Korman MH, Jakubczak JL, Eickbush TH. Reverse transcription of R2Bm RNA is primed by a nick at the chromosomal target site: a mechanism for non-LTR retrotransposition. Cell. 1993;72:595–605. doi: 10.1016/0092-8674(93)90078-5. [DOI] [PubMed] [Google Scholar] source
Not checked in the free run.
- cites [7] Luan DD, Eickbush TH. RNA template requirements for target DNA-primed reverse transcription by the R2 retrotransposable element. Mol. Cell. Biol. 1995;15:3882–3891. doi: 10.1128/mcb.15.7.3882. [DOI] [PMC free article] [PubMed] [Google Scholar] source
Not checked in the free run.
May combine two claims.
Interpretationreasoning§ DiscussionNon-LTR retrotransposons encode protein machinery that initiates insertion into DNA but largely requires host factors for many subsequent steps.
“This last report and our results demonstrate that non-LTR retrotransposons encode protein machinery that initiates insertion into DNA but largely requires host factors for many of the subsequent steps.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Interpretationreasoning§ DiscussionThe ATM requirement for L1 integration could have potential consequences for human health in ATM-compromised individuals.
“The ATM requirement for L1 integration could have potential consequences for human health in ATM-compromised individuals.”
Quote in the paperNot a substantial claimMay combine two claims.
Interpretationown data§ DiscussionThis work demonstrates that the L1 integration process produces DSBs and requires a DSB-repair protein.
“This work demonstrates that the L1 integration process produces DSBs and requires a DSB-repair protein.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim. May combine two claims.
Interpretationreasoning§ DiscussionBecause non-LTR insertion proceeds through a different integration mechanism in which cDNA synthesis precedes endonuclease activity, this dependence represents a novel understanding of the L1 life cycle.
“Because non-LTR insertion proceeds through a different integration mechanism in which cDNA synthesis precedes endonuclease activity, this dependence represents a novel understanding of the L1 life cycle.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductcitation§ Materials and MethodsThe COMET assay used in this study is based on the method outlined by Singh et al.
“The COMET assay is based on the method outlined by Singh et al.53”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Singh et al.53 Singh NP, McCoy MT, Tice RR, Schneider EL. A simple technique for quantitation of low levels of DNA damage in individual cells. Expt. Cell Res. 1988;175:184–191. doi: 10.1016/0014-4827(88)90265-0. [DOI] [PubMed] [Google Scholar]
Not checked in the free run.
Classified as probably not a substantial claim.
Premisecitation§ IntroductionL1 utilizes an APE-like endonuclease to insert into target DNA.
“L1 utilizes an APE-like endonuclease to insert into the target DNA.5”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [5] Feng Q, Moran JV, Kazazian HH, Jr, Boeke JD. Human L1 retrotransposon encodes a conserved endonuclease required for retrotransposition. Cell. 1996;87:905–916. doi: 10.1016/s0092-8674(00)81997-2. [DOI] [PubMed] [Google Scholar] source
Not checked in the free run.
Classified as probably not a substantial claim.
Interpretationreasoning§ IntroductionIn TPRT models, cleavage of both strands of genomic DNA is required, implying an intermediate equivalent to a DSB is present during integration.
“In these models of TPRT, cleavage of both strands of genomic DNA is required, which implies that an intermediate equivalent to a DSB is present during the integration process.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationreasoning§ DiscussionThe L1 endonuclease may be responsible for insertion of the dispersed sites of homology, as well as creating the DSBs adjacent to them that facilitate instability.
“Thus, the L1 endonuclease may be responsible for insertion of the dispersed sites of homology, as well as creating the DSBs adjacent to them that facilitate the instability.”
Quote in the paperSubstantial claim
The paper relies on this without support.
The DSB formation observed from transfected L1 expression reflects the behavior of endogenously expressed L1 elements.
“This result suggests that the endonuclease activity of endogenously expressed L1 elements could contribute to DSB formation in germ-line and somatic tissues.”
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?
DNA lesions, in particular dsDNA breaks, can arise as collateral damage associated with retrotransposition.
“DNA lesions, in particular dsDNA breaks (DSB), can arise as ‘collateral damage’ associated with retrotransposition19, 20, 102.”
From The role of retrotransposable elements in ageing and age-associated diseases (2021) · cites this paper as [102]
Ectopic retrotransposon activation has been associated with DNA damage and genomic instability.
“Since ectopic retrotransposon activation has been associated with DNA damage and genomic instability (87, 90)”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [90]
L1 retrotransposon activity has been linked to DNA damage, mutagenesis, and deregulation of host gene transcription.
“Long interspersed element 1 (L1) retrotransposon activity, in particular, has been linked to DNA damage5, mutagenesis6,7, and deregulation of host gene transcription8.”
From SIRT6 represses LINE1 retrotransposons by ribosylating KAP1 but this repression fails with stress and age (2014) · cites this paper as [5]
Locus-specific DNA hypermethylation is associated with ageing blood and tissues and appears to be conserved between mice, monkeys and humans.
“In addition, locus-specific DNA hypermethylation has been associated with ageing blood and tissues 52,53 and appears to be conserved between mice, monkeys and humans 54 .”
From The roles of DNA, RNA and histone methylation in ageing and cancer (2019) · cites this paper as [54]
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- Authors
- Gasior, S. L., Wakeman, T. P., Xu, B., & Deininger, P. L.
- Affiliations
- Tulane University (US)
- Louisiana State University (US)
- Corresponding author
- Deininger, Prescott L.
- Venue
- Journal of Molecular Biology
- Publisher
- Elsevier BV
- Published
- 2006-04
- Volume
- 357
- Issue
- 5
- Pages
- 1383-1393
- ISSN
- 0022-2836 (ISSN-L)
- PMC
- PMC4136747
- OpenAlex
- W1987332588
- Semantic Scholar
- 0eebb3ad93ef9c873e76a6294c3d89270c042f53
- Cited by
- 519
- References
- 90
- Citations by year
- 2026: 26 · 2025: 31 · 2024: 33 · 2023: 30 · 2022: 35 · 2021: 35 · 2020: 28 · 2019: 21 · 2018: 26 · 2017: 20 · 2016: 22 · 2015: 27 · 2014: 27 · 2013: 30 · 2012: 26
- FWCI
- 25.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Journal of Molecular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Science Foundation (EPS-0346411)
- U.S. Public Health Service (R01GM45668)
- National Institutes of Health
- U.S. Department of Defense (DAM 17-03-1-0709)
- American Cancer Society
- Brown Foundation
- Louisiana Board of Regents (P20RR020152-01, R03ES013301-01)
- Topics
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Chromosomal and Genetic Variations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
- Keywords
- LINE-1 retrotransposons, DNA double-strand breaks, retrotransposition, ATM, γH2AX foci, DNA repair, endonuclease activity, non-LTR retrotransposons, human genome
- MeSH terms
- Animals, Cell Cycle, DNA, DNA Damage, DNA Repair, DNA-Binding Proteins, HeLa Cells, Histones, Humans, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Long Interspersed Nucleotide Elements, Comet Assay, Tumor Suppressor Proteins, DNA Fragmentation, Ataxia Telangiectasia Mutated Proteins
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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.
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