Identification of an XRCC1 DNA binding activity essential for retention at sites of DNA damage
Author:
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/s41598-019-39543-1.pdf
Reference44 articles.
1. Thompson, L. H. & West, M. G. XRCC1 keeps DNA from getting stranded. Mutat. Res. 459, 1–18, https://doi.org/10.1016/S0921-8777(99)00058-0 (2000).
2. Almeida, K. H. & Sobol, R. W. A unified view of base excision repair: lesion-dependent protein complexes regulated by post-translational modification. DNA Repair 6, 695–711, https://doi.org/10.1016/j.dnarep.2007.01.009 (2007).
3. Thompson, L. H. et al. A CHO-cell strain having hypersensitivity to mutagens, a defect in DNA strand-break repair, and an extraordinary baseline frequency of sister-chromatid exchange. Mutation Research 95, 427–440, https://doi.org/10.1016/0027-5107(82)90276-7 (1982).
4. Thompson, L. H., Brookman, K. W., Jones, N. J., Allen, S. A. & Carrano, A. V. Molecular cloning of the human XRCC1 gene, which corrects defective DNA strand break repair and sister chromatid exchange. Mol. Cell. Biol. 10, 6160–6171, https://doi.org/10.1128/MCB.10.12.6160 (1990).
5. Tebbs, R. S. et al. Requirement for the XRCC1 DNA base excision repair gene during early mouse development. Developmental Biology 208, 513–529, https://doi.org/10.1006/dbio.1999.9232 (1999).
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