The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations
Open accessAbstract
We have used spectral karyotyping to assess potential roles of three different components of the nonhomologous DNA end-joining pathway in the maintenance of genomic stability in mouse embryonic fibroblasts (MEFs). MEFs homozygous for mutations that inactivate either DNA ligase IV (Lig4) or Ku70 display dramatic genomic instability, even in the absence of exogenous DNA damaging agents. These aberrant events range from chromosomal fragmentation to nonreciprocal translocations that can involve several chromosomes. DNA-dependent protein kinase catalytic subunit deficiency also promotes genome instability. Deficiency for the p53 cell cycle checkpoint protein has little effect on spontaneous levels of chromosomal instability in Lig4-deficient fibroblasts. However, in the context of ionizing radiation treatment, p53 deficiency allowed visualization of massive acute chromosomal destruction in Lig4-deficient MEFs, which in surviving cells manifested as frequent nonreciprocal translocations. We conclude that nonhomologous DNA end-joining plays a crucial role as a caretaker of the mammalian genome, and that an alternative repair pathway exists that often leads to nonreciprocal translocations.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
The double-strand-break repair model for recombination
Szostak, J. W., Orr-Weaver, T. L., Rothstein, R. J., & Stahl, F. W. (1983) · Cell · doi:10.1016/0092-8674(83)90331-8 · Cited by 2,437
Takata, M., Sasaki, M. S., Sonoda, E., Morrison, C., Hashimoto, M., Utsumi, H., Yamaguchi‐Iwai, Y., Shinohara, A., & Takeda, S. (1998) · The EMBO Journal · doi:10.1093/emboj/17.18.5497 · Cited by 1,229
Rad51-deficient vertebrate cells accumulate chromosomal breaks prior to cell death
Sonoda, E. (1998) · The EMBO Journal · doi:10.1093/emboj/17.2.598 · Cited by 791
A critical role for DNA end-joining proteins in both lymphogenesis and neurogenesis
Gao, Y., Sun, Y., Frank, K. M., Dikkes, P., Fujiwara, Y., Seidl, K. J., Sekiguchi, J. M., Rathbun, G. A., Swat, W., Wang, J., et al. (1998) · Cell · doi:10.1016/s0092-8674(00)81714-6 · Cited by 688
Self-citationRequirement for Ku80 in growth and immunoglobulin V(D)J recombination
Nussenzweig, A., Chen, C., da Costa Soares, V., Sanchez, M., Sokol, K., Nussenzweig, M. C., & Li, G. C. (1996) · Nature · doi:10.1038/382551a0 · Cited by 663
Homology-directed repair is a major double-strand break repair pathway in mammalian cells
Liang, F., Han, M., Romanienko, P. J., & Jasin, M. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.9.5172 · Cited by 649
Late embryonic lethality and impaired V (D)J recombination in mice lacking DNA ligase IV
Frank, K. M., Sekiguchi, J. M., Seidl, K. J., Swat, W., Rathbun, G. A., Cheng, H.-L., Davidson, L., Kangaloo, L., & Alt, F. W. (1998) · Nature · doi:10.1038/24172 · Cited by 594
Self-citationInterplay of p53 and DNA-repair protein XRCC4 in tumorigenesis, genomic stability and development
Gao, Y., Ferguson, D. O., Xie, W., Manis, J. P., Sekiguchi, J., Frank, K. M., Chaudhuri, J., Horner, J., DePinho, R. A., & Alt, F. W. (2000) · Nature · doi:10.1038/35009138 · Cited by 580
Self-citationEfficient copying of nonhomologous sequences from ectopic sites via P-element-induced gap repair.
Nassif, N., Penney, J., Pal, S., Engels, W. R., & Gloor, G. B. (1994) · Molecular and Cellular Biology · doi:10.1128/mcb.14.3.1613 · Cited by 460
Cited by
DNA double-strand break repair-pathway choice in somatic mammalian cells
Scully, R., Panday, A., Elango, R., & Willis, N. A. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0152-0 · Cited by 1,457
Genomic Instability in Mice Lacking Histone H2AX
Celeste, A., Petersen, S., Romanienko, P. J., Fernandez-Capetillo, O., Chen, H. T., Sedelnikova, O. A., Reina-San-Martin, B., Coppola, V., Meffre, E., Difilippantonio, M. J., et al. (2002) · Science · doi:10.1126/science.1069398 · Cited by 1,385
Regulation of DNA double-strand break repair pathway choice
Shrivastav, M., De Haro, L. P., & Nickoloff, J. A. (2008) · Cell Research · doi:10.1038/cr.2007.111 · Cited by 1,329
Chromosomal stability and the DNA double-stranded break connection
van Gent, D. C., Hoeijmakers, J. H. J., & Kanaar, R. (2001) · Nature Reviews Genetics · doi:10.1038/35056049 · Cited by 1,219
MMEJ repair of double-strand breaks (director’s cut): deleted sequences and alternative endings
McVey, M., & Lee, S. E. (2008) · Trends in Genetics · doi:10.1016/j.tig.2008.08.007 · Cited by 986
Metadata
- Authors
- Ferguson, D. O., Sekiguchi, J. M., Chang, S., Frank, K. M., Gao, Y., DePinho, R. A., & Alt, F. W.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2000-05-23
- Volume
- 97
- Issue
- 12
- Pages
- 6630-6633
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1986320226
- Cited by
- 356
- References
- 35
- FWCI
- 8.34
- Type
- journal article
- Language
- en
- Open access
- green
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.
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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations. https://app.cochat.ai/papers/10.1073/pnas.110152897
- The paper
- Ferguson, D. O., Sekiguchi, J. M., Chang, S., Frank, K. M., Gao, Y., DePinho, R. A., & Alt, F. W. (2000). The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.110152897
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
