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BRCA1 Is Required for Postreplication Repair after UV-Induced DNA Damage
BRCA1 contributes to the response to UV irradiation. Utilizing its BRCT motifs, it is recruited during S/G2 to UV-damaged sites in a DNA replication-dependent but nucleotide excision repair (NER)-independent manner. More specifically, at UV-stalled replication forks, it promotes photoproduct excisio...
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Published in: | Molecular cell 2011-10, Vol.44 (2), p.235-251 |
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container_title | Molecular cell |
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creator | Pathania, Shailja Nguyen, Jenna Hill, Sarah J. Scully, Ralph Adelmant, Guillaume O. Marto, Jarrod A. Feunteun, Jean Livingston, David M. |
description | BRCA1 contributes to the response to UV irradiation. Utilizing its BRCT motifs, it is recruited during S/G2 to UV-damaged sites in a DNA replication-dependent but nucleotide excision repair (NER)-independent manner. More specifically, at UV-stalled replication forks, it promotes photoproduct excision, suppression of translesion synthesis, and the localization and activation of replication factor C complex (RFC) subunits. The last function, in turn, triggers post-UV checkpoint activation and postreplicative repair. These BRCA1 functions differ from those required for DSBR.
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► BRCA1 promotes resistance to UV damage and concentrates at UV-stalled forks ► BRCA1-dependent localization of RFC at UV-stalled forks contributes to their repair ► BRCA1/RFC/9-1-1 interactions contribute to post-UV G2/M checkpoint activation ► BRCA1 suppresses translesional synthesis in UV-damaged cells |
doi_str_mv | 10.1016/j.molcel.2011.09.002 |
format | article |
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► BRCA1 promotes resistance to UV damage and concentrates at UV-stalled forks ► BRCA1-dependent localization of RFC at UV-stalled forks contributes to their repair ► BRCA1/RFC/9-1-1 interactions contribute to post-UV G2/M checkpoint activation ► BRCA1 suppresses translesional synthesis in UV-damaged cells</description><identifier>ISSN: 1097-2765</identifier><identifier>EISSN: 1097-4164</identifier><identifier>DOI: 10.1016/j.molcel.2011.09.002</identifier><identifier>PMID: 21963239</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>BRCA1 Protein - genetics ; BRCA1 Protein - metabolism ; Cell Line ; DNA ; DNA Breaks, Double-Stranded ; DNA Damage ; DNA repair ; DNA Repair - physiology ; DNA Replication ; Humans ; replication ; Replication Protein C - genetics ; Replication Protein C - metabolism ; tumor suppressor proteins ; ultraviolet radiation ; Ultraviolet Rays</subject><ispartof>Molecular cell, 2011-10, Vol.44 (2), p.235-251</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-b56d002f49258bd05793605ad2ff5e712c2a5ef6835af12053e87dcad37c3ec73</citedby><cites>FETCH-LOGICAL-c496t-b56d002f49258bd05793605ad2ff5e712c2a5ef6835af12053e87dcad37c3ec73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21963239$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pathania, Shailja</creatorcontrib><creatorcontrib>Nguyen, Jenna</creatorcontrib><creatorcontrib>Hill, Sarah J.</creatorcontrib><creatorcontrib>Scully, Ralph</creatorcontrib><creatorcontrib>Adelmant, Guillaume O.</creatorcontrib><creatorcontrib>Marto, Jarrod A.</creatorcontrib><creatorcontrib>Feunteun, Jean</creatorcontrib><creatorcontrib>Livingston, David M.</creatorcontrib><title>BRCA1 Is Required for Postreplication Repair after UV-Induced DNA Damage</title><title>Molecular cell</title><addtitle>Mol Cell</addtitle><description>BRCA1 contributes to the response to UV irradiation. Utilizing its BRCT motifs, it is recruited during S/G2 to UV-damaged sites in a DNA replication-dependent but nucleotide excision repair (NER)-independent manner. More specifically, at UV-stalled replication forks, it promotes photoproduct excision, suppression of translesion synthesis, and the localization and activation of replication factor C complex (RFC) subunits. The last function, in turn, triggers post-UV checkpoint activation and postreplicative repair. These BRCA1 functions differ from those required for DSBR.
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► BRCA1 promotes resistance to UV damage and concentrates at UV-stalled forks ► BRCA1-dependent localization of RFC at UV-stalled forks contributes to their repair ► BRCA1/RFC/9-1-1 interactions contribute to post-UV G2/M checkpoint activation ► BRCA1 suppresses translesional synthesis in UV-damaged cells</description><subject>BRCA1 Protein - genetics</subject><subject>BRCA1 Protein - metabolism</subject><subject>Cell Line</subject><subject>DNA</subject><subject>DNA Breaks, Double-Stranded</subject><subject>DNA Damage</subject><subject>DNA repair</subject><subject>DNA Repair - physiology</subject><subject>DNA Replication</subject><subject>Humans</subject><subject>replication</subject><subject>Replication Protein C - genetics</subject><subject>Replication Protein C - metabolism</subject><subject>tumor suppressor proteins</subject><subject>ultraviolet radiation</subject><subject>Ultraviolet Rays</subject><issn>1097-2765</issn><issn>1097-4164</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqNkctu1DAUQC0EoqXwBwiyg02C3443SMMU6EgVoMKwtTz2deVRMp7aCRJ_j6sMLCu8saV77sP3IPSS4I5gIt_tuzENDoaOYkI6rDuM6SN0TrBWLSeSPz69qZLiDD0rZY8x4aLXT9EZJVoyyvQ5uvpws16RZlOaG7ibYwbfhJSbb6lMGY5DdHaK6VCDRxtzY8MEudn-bDcHP7vKXn5ZNZd2tLfwHD0Jdijw4nRfoO2njz_WV-3118-b9eq6dVzLqd0J6euggWsq-p3HQmkmsbCehiBAEeqoFRBkz4QNhGLBoFfeWc-UY-AUu0BvlrrHnO5mKJMZY6lrGOwB0lyMxoooTgT9DxJL1jPOK_n2QZLiegRhVFaUL6jLqZQMwRxzHG3-bQg2917M3ixezL0Xg7Wp361pr04d5t0I_l_SXxEVeL0AwSZjb3MsZvu9VpC1MxFc9ZV4vxBQt_srQjbFRThUC9Wam4xP8eEZ_gA9ZKYy</recordid><startdate>20111021</startdate><enddate>20111021</enddate><creator>Pathania, Shailja</creator><creator>Nguyen, Jenna</creator><creator>Hill, Sarah J.</creator><creator>Scully, Ralph</creator><creator>Adelmant, Guillaume O.</creator><creator>Marto, Jarrod A.</creator><creator>Feunteun, Jean</creator><creator>Livingston, David M.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7S9</scope><scope>L.6</scope><scope>7X8</scope><scope>7TM</scope></search><sort><creationdate>20111021</creationdate><title>BRCA1 Is Required for Postreplication Repair after UV-Induced DNA Damage</title><author>Pathania, Shailja ; 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Utilizing its BRCT motifs, it is recruited during S/G2 to UV-damaged sites in a DNA replication-dependent but nucleotide excision repair (NER)-independent manner. More specifically, at UV-stalled replication forks, it promotes photoproduct excision, suppression of translesion synthesis, and the localization and activation of replication factor C complex (RFC) subunits. The last function, in turn, triggers post-UV checkpoint activation and postreplicative repair. These BRCA1 functions differ from those required for DSBR.
[Display omitted]
► BRCA1 promotes resistance to UV damage and concentrates at UV-stalled forks ► BRCA1-dependent localization of RFC at UV-stalled forks contributes to their repair ► BRCA1/RFC/9-1-1 interactions contribute to post-UV G2/M checkpoint activation ► BRCA1 suppresses translesional synthesis in UV-damaged cells</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>21963239</pmid><doi>10.1016/j.molcel.2011.09.002</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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subjects | BRCA1 Protein - genetics BRCA1 Protein - metabolism Cell Line DNA DNA Breaks, Double-Stranded DNA Damage DNA repair DNA Repair - physiology DNA Replication Humans replication Replication Protein C - genetics Replication Protein C - metabolism tumor suppressor proteins ultraviolet radiation Ultraviolet Rays |
title | BRCA1 Is Required for Postreplication Repair after UV-Induced DNA Damage |
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