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- W2123258564 abstract "TRF1 protects mammalian telomeres from fusion and fragility. Depletion of TRF1 leads to telomere fusions as well as accumulation of γ-H2AX foci and activation of both the ataxia telangiectasia mutated (ATM)- and the ataxia telangiectasia and Rad3 related (ATR)-mediated deoxyribonucleic acid (DNA) damage response (DDR) pathways. 53BP1, which is also present at dysfunctional telomeres, is a target of ATM that accumulates at DNA double-strand breaks and favors nonhomologous end-joining (NHEJ) repair over ATM-dependent resection and homology-directed repair (homologous recombination [HR]). To address the role of 53BP1 at dysfunctional telomeres, we generated mice lacking TRF1 and 53BP1. 53BP1 deficiency significantly rescued telomere fusions in mouse embryonic fibroblasts (MEFs) lacking TRF1, but they showed evidence of a switch from the NHEJ- to HR-mediated repair of uncapped telomeres. Concomitantly, double-mutant MEFs showed evidence of hyperactivation of the ATR-dependent DDR. In intact mice, combined 53BP1/TRF1 deficiency in stratified epithelia resulted in earlier onset of DNA damage and increased CHK1 phosphorylation during embryonic development, leading to aggravation of skin phenotypes." @default.
- W2123258564 created "2016-06-24" @default.
- W2123258564 creator A5017520712 @default.
- W2123258564 creator A5070199101 @default.
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- W2123258564 date "2012-04-16" @default.
- W2123258564 modified "2023-10-03" @default.
- W2123258564 title "53BP1 deficiency combined with telomere dysfunction activates ATR-dependent DNA damage response" @default.
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- W2123258564 cites W1726562753 @default.
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- W2123258564 cites W1970266671 @default.
- W2123258564 cites W1970891016 @default.
- W2123258564 cites W1972655555 @default.
- W2123258564 cites W1977488724 @default.
- W2123258564 cites W1979385111 @default.
- W2123258564 cites W1981525849 @default.
- W2123258564 cites W1982006042 @default.
- W2123258564 cites W1987369963 @default.
- W2123258564 cites W1987615467 @default.
- W2123258564 cites W1988530580 @default.
- W2123258564 cites W1990507848 @default.
- W2123258564 cites W1990850872 @default.
- W2123258564 cites W1993026474 @default.
- W2123258564 cites W1999796994 @default.
- W2123258564 cites W2003673006 @default.
- W2123258564 cites W2004173334 @default.
- W2123258564 cites W2007369689 @default.
- W2123258564 cites W2007919127 @default.
- W2123258564 cites W2015414930 @default.
- W2123258564 cites W2018182154 @default.
- W2123258564 cites W2027379868 @default.
- W2123258564 cites W2027779909 @default.
- W2123258564 cites W2027960166 @default.
- W2123258564 cites W2033200608 @default.
- W2123258564 cites W2033230283 @default.
- W2123258564 cites W2035389897 @default.
- W2123258564 cites W2040392790 @default.
- W2123258564 cites W2043895957 @default.
- W2123258564 cites W2047144239 @default.
- W2123258564 cites W2048109276 @default.
- W2123258564 cites W2048228863 @default.
- W2123258564 cites W2049262839 @default.
- W2123258564 cites W2053844006 @default.
- W2123258564 cites W2058375396 @default.
- W2123258564 cites W2059574913 @default.
- W2123258564 cites W2062284662 @default.
- W2123258564 cites W2068973408 @default.
- W2123258564 cites W2072744580 @default.
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- W2123258564 cites W2146106370 @default.
- W2123258564 cites W2147765162 @default.
- W2123258564 cites W2149718327 @default.
- W2123258564 cites W2150490516 @default.
- W2123258564 cites W2153633026 @default.
- W2123258564 cites W2157899948 @default.
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- W2123258564 cites W2161232591 @default.
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- W2123258564 cites W2167368071 @default.
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- W2123258564 doi "https://doi.org/10.1083/jcb.201110124" @default.
- W2123258564 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3328378" @default.
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- W2123258564 hasPublicationYear "2012" @default.
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