53BP1: pro choice in DNA repair

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Authors

ZIMMERMANN Michal DE LANGE T.

Year of publication 2014
Type Article in Periodical
Magazine / Source TRENDS IN CELL BIOLOGY
MU Faculty or unit

Central European Institute of Technology

Citation
Web http://ac.els-cdn.com/S0962892413001554/1-s2.0-S0962892413001554-main.pdf?_tid=66e12f66-bb3a-11e4-abe9-00000aacb360&acdnat=1424682203_f8bd4c3cd228cef3ed42bebd7ad4b631
Doi http://dx.doi.org/10.1016/j.tcb.2013.09.003
Field Genetics and molecular biology
Keywords 53BP1; Rif1; PTIP; NHEJ; HDR; PARPi; telomere; CSR; V(D)J; BRCA1; resection
Description The DNA damage response factor 53BP1 functions at the intersection of two major double strand break (DSB) repair pathways - promoting nonhomologous end-joining (NHEJ) and inhibiting homology-directed repair (HDR) - and integrates cellular inputs to ensure their timely execution in the proper cellular contexts. Recent work has revealed that 53BP1 controls 5' end resection at DNA ends, mediates synapsis of DNA ends, promotes the mobility of damaged chromatin, improves DSB repair in heterochromatic regions, and contributes to lethal mis-repair of DSBs in BRCA1-deficient cells. Here we review these aspects of 53BP1 and discuss new data revealing how 53BP1 is loaded onto chromatin and uses its interacting factors Rif1 and PTIP to promote NHEJ and inhibit HDR.
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