CtIP-mediated fork protection synergizes with BRCA1 to suppress genomic instability upon DNA replication stress. Przetocka et al

Main Author: Sartori, Alessandro
Format: Dataset
Terbitan: Mendeley , 2018
Subjects:
Online Access: https:/data.mendeley.com/datasets/vfpfxkbcbd
ctrlnum 0.17632-vfpfxkbcbd.1
fullrecord <?xml version="1.0"?> <dc><creator>Sartori, Alessandro</creator><title>CtIP-mediated fork protection synergizes with BRCA1 to suppress genomic instability upon DNA replication stress. Przetocka et al</title><publisher>Mendeley</publisher><description>In this study, we report a previously unrecognized function of CtIP in maintaining replication fork stability that is distinct from its role in DSB resection. In brief, we show that CtIP keeps DNA2 nuclease in check to limit degradation of stalled forks. Moreover, we find that loss of CtIP in BRCA1-deficient cells aggravates replication stress-induced genomic instability, causing synthetic lethality.</description><subject>Molecular Biology</subject><type>Other:Dataset</type><identifier>10.17632/vfpfxkbcbd.1</identifier><rights>Creative Commons Attribution 4.0 International</rights><rights>http://creativecommons.org/licenses/by/4.0</rights><relation>https:/data.mendeley.com/datasets/vfpfxkbcbd</relation><date>2018-09-13T15:51:57Z</date><date>2018-10-18T00:00:00Z</date><recordID>0.17632-vfpfxkbcbd.1</recordID></dc>
format Other:Dataset
Other
author Sartori, Alessandro
title CtIP-mediated fork protection synergizes with BRCA1 to suppress genomic instability upon DNA replication stress. Przetocka et al
publisher Mendeley
publishDate 2018
topic Molecular Biology
url https:/data.mendeley.com/datasets/vfpfxkbcbd
contents In this study, we report a previously unrecognized function of CtIP in maintaining replication fork stability that is distinct from its role in DSB resection. In brief, we show that CtIP keeps DNA2 nuclease in check to limit degradation of stalled forks. Moreover, we find that loss of CtIP in BRCA1-deficient cells aggravates replication stress-induced genomic instability, causing synthetic lethality.
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