Non-catalytic Roles for XPG with BRCA1 and BRCA2 in Homologous Recombination and Genome Stability

Autor: Jan H.J. Hoeijmakers, Priscilla K. Cooper, Brian Shih, Ann C. Parplys, Miaw Sheue Tsai, Torsten Groesser, Kelly S. Trego, Janice M. Pluth, Ayesu Hlaing, Michael R. Nelson, Weixing Zhao, Patrick Sung, Claudia Wiese, Albert R. Davalos, Björn Rydberg, Judith Campisi

Publikováno v: Trego, K S, Groesser, T, Davalos, A R, Parplys, A C, Zhao, W, Nelson, M R, Hlaing, A, Shih, B, Rydberg, B, Pluth, J M, Tsai, M-S, Hoeijmakers, J H J, Sung, P, Wiese, C, Campisi, J & Cooper, P K 2016, ' Non-catalytic Roles for XPG with BRCA1 and BRCA2 in Homologous Recombination and Genome Stability ', Molecular Cell, vol. 61, pp. 535–546 . https://doi.org/10.1016/j.molcel.2015.12.026
Molecular cell, vol 61, iss 4
Trego, KS; Groesser, T; Davalos, AR; Parplys, AC; Zhao, W; Nelson, MR; et al.(2016). Non-catalytic Roles for XPG with BRCA1 and BRCA2 in Homologous Recombination and Genome Stability. Molecular Cell, 61(4), 535-546. doi: 10.1016/j.molcel.2015.12.026. Lawrence Berkeley National Laboratory: Lawrence Berkeley National Laboratory. Retrieved from: http://www.escholarship.org/uc/item/2618t9h0
Molecular Cell, 61(4), 535-546. Cell Press

© 2016 Elsevier Inc. XPG is a structure-specific endonuclease required for nucleotide excision repair, and incision-defective XPG mutations cause the skin cancer-prone syndrome xeroderma pigmentosum. Truncating mutations instead cause the neurodevel

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https://doi.org/10.1016/j.molcel.2015.12.026