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Cited by 368

The DOI matches its Crossref record; 113 of the 113 references it cites were found in a registry or an index.

53BP1: pro choice in DNA repair

Open access
Zimmermann, Michal, de Lange, Titia·2014·Trends in Cell Biology

Abstract

The DNA damage response factor 53BP1 functions at the intersection of two major double strand break (DSB) repair pathways – promoting non-homologous 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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Metadata

Authors
Zimmermann, M., & de Lange, T.
Venue
Trends in Cell Biology
Publisher
Elsevier BV
Published
2014-02
Volume
24
Issue
2
Pages
108-117
ISSN
0962-8924 (ISSN-L)
OpenAlex
W2077399723
Cited by
368
References
113
FWCI
1.88
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: 53BP1: pro choice in DNA repair. https://app.cochat.ai/papers/10.1016/j.tcb.2013.09.003
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Zimmermann, M., & de Lange, T. (2014). 53BP1: pro choice in DNA repair. Trends in Cell Biology. https://doi.org/10.1016/j.tcb.2013.09.003

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