The differences between ICL repair during and outside of S phase
•Interstrand crosslinks are repaired by distinct pathways during and outside of S phase.•ICL repair outside of S phase is critical for cellular homeostasis, particularly in postmitotic or rarely dividing cells. DNA interstrand crosslinks (ICLs) are complex lesions that block essential DNA transactio...
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Veröffentlicht in: | Trends in biochemical sciences (Amsterdam. Regular ed.) 2013-08, Vol.38 (8), p.386-393 |
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creator | Williams, Hannah L. Gottesman, Max E. Gautier, Jean |
description | •Interstrand crosslinks are repaired by distinct pathways during and outside of S phase.•ICL repair outside of S phase is critical for cellular homeostasis, particularly in postmitotic or rarely dividing cells.
DNA interstrand crosslinks (ICLs) are complex lesions that block essential DNA transactions including DNA replication, recombination, and RNA transcription. Naturally occurring ICLs are rare, yet these lesions are the major cause of toxicity following treatment with several classes of crosslinking cancer chemotherapeutic drugs. ICLs are repaired during and outside of S phase by pathways with overlapping as well as distinct features. Here, we discuss some recent insights into the mechanisms of replication-dependent and replication-independent repair of ICLs with special emphasis on the differences between these repair pathways. |
doi_str_mv | 10.1016/j.tibs.2013.05.004 |
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DNA interstrand crosslinks (ICLs) are complex lesions that block essential DNA transactions including DNA replication, recombination, and RNA transcription. Naturally occurring ICLs are rare, yet these lesions are the major cause of toxicity following treatment with several classes of crosslinking cancer chemotherapeutic drugs. ICLs are repaired during and outside of S phase by pathways with overlapping as well as distinct features. Here, we discuss some recent insights into the mechanisms of replication-dependent and replication-independent repair of ICLs with special emphasis on the differences between these repair pathways.</description><identifier>ISSN: 0968-0004</identifier><identifier>EISSN: 1362-4326</identifier><identifier>DOI: 10.1016/j.tibs.2013.05.004</identifier><identifier>PMID: 23830640</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Antineoplastic Agents - adverse effects ; Cell Cycle ; Cross-Linking Reagents - adverse effects ; Cross-Linking Reagents - toxicity ; crosslinking ; DNA ; DNA Damage ; DNA Repair ; DNA Repair Enzymes - metabolism ; DNA replication ; drug therapy ; drugs ; Humans ; interphase ; Models, Biological ; Recombinational DNA Repair ; RNA ; S Phase ; toxicity</subject><ispartof>Trends in biochemical sciences (Amsterdam. Regular ed.), 2013-08, Vol.38 (8), p.386-393</ispartof><rights>2013 Elsevier Ltd</rights><rights>Copyright © 2013 Elsevier Ltd. All rights reserved.</rights><rights>2013 Elsevier Ltd. All rights reserved. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-5e8f8ef3b013ee48edd5455964f9f0e6b2ef05a2d262fe9e7f23150a8d776df93</citedby><cites>FETCH-LOGICAL-c512t-5e8f8ef3b013ee48edd5455964f9f0e6b2ef05a2d262fe9e7f23150a8d776df93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S096800041300090X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23830640$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Williams, Hannah L.</creatorcontrib><creatorcontrib>Gottesman, Max E.</creatorcontrib><creatorcontrib>Gautier, Jean</creatorcontrib><title>The differences between ICL repair during and outside of S phase</title><title>Trends in biochemical sciences (Amsterdam. Regular ed.)</title><addtitle>Trends Biochem Sci</addtitle><description>•Interstrand crosslinks are repaired by distinct pathways during and outside of S phase.•ICL repair outside of S phase is critical for cellular homeostasis, particularly in postmitotic or rarely dividing cells.
DNA interstrand crosslinks (ICLs) are complex lesions that block essential DNA transactions including DNA replication, recombination, and RNA transcription. Naturally occurring ICLs are rare, yet these lesions are the major cause of toxicity following treatment with several classes of crosslinking cancer chemotherapeutic drugs. ICLs are repaired during and outside of S phase by pathways with overlapping as well as distinct features. Here, we discuss some recent insights into the mechanisms of replication-dependent and replication-independent repair of ICLs with special emphasis on the differences between these repair pathways.</description><subject>Animals</subject><subject>Antineoplastic Agents - adverse effects</subject><subject>Cell Cycle</subject><subject>Cross-Linking Reagents - adverse effects</subject><subject>Cross-Linking Reagents - toxicity</subject><subject>crosslinking</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>DNA Repair</subject><subject>DNA Repair Enzymes - metabolism</subject><subject>DNA replication</subject><subject>drug therapy</subject><subject>drugs</subject><subject>Humans</subject><subject>interphase</subject><subject>Models, Biological</subject><subject>Recombinational DNA Repair</subject><subject>RNA</subject><subject>S Phase</subject><subject>toxicity</subject><issn>0968-0004</issn><issn>1362-4326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1DAURi0EokPhBViAl2wSru3YcSSEikb8VBqJRdu15cTXMx7NxIOdFPH2OJpSwYaVJfvc7346JuQ1g5oBU-_39RT6XHNgogZZAzRPyIoJxatGcPWUrKBTuoJyf0Fe5LwHYLJt5XNywYUWoBpYkavbHVIXvMeE44CZ9jj9RBzp9XpDE55sSNTNKYxbakdH4zzl4JBGT2_oaWczviTPvD1kfPVwXpK7L59v19-qzfev1-tPm2qQjE-VRO01etGXsoiNRudkI2WnGt95QNVz9CAtd1xxjx22ngsmwWrXtsr5TlySj-fc09wf0Q04TskezCmFo02_TLTB_Psyhp3ZxnsjWiU63pSAdw8BKf6YMU_mGPKAh4MdMc7Z8CIKdKeZLCg_o0OKOSf0j2sYmEW92ZtFvVnUG5CmKC5Db_4u-Djyx3UB3p4Bb6Ox2xSyubspCWpZLEAvxIczgUXkfcBk8hCWb3Eh4TAZF8P_GvwGXcSecw</recordid><startdate>20130801</startdate><enddate>20130801</enddate><creator>Williams, Hannah L.</creator><creator>Gottesman, Max E.</creator><creator>Gautier, Jean</creator><general>Elsevier Ltd</general><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>5PM</scope></search><sort><creationdate>20130801</creationdate><title>The differences between ICL repair during and outside of S phase</title><author>Williams, Hannah L. ; Gottesman, Max E. ; Gautier, Jean</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-5e8f8ef3b013ee48edd5455964f9f0e6b2ef05a2d262fe9e7f23150a8d776df93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - adverse effects</topic><topic>Cell Cycle</topic><topic>Cross-Linking Reagents - adverse effects</topic><topic>Cross-Linking Reagents - toxicity</topic><topic>crosslinking</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>DNA Repair</topic><topic>DNA Repair Enzymes - metabolism</topic><topic>DNA replication</topic><topic>drug therapy</topic><topic>drugs</topic><topic>Humans</topic><topic>interphase</topic><topic>Models, Biological</topic><topic>Recombinational DNA Repair</topic><topic>RNA</topic><topic>S Phase</topic><topic>toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Williams, Hannah L.</creatorcontrib><creatorcontrib>Gottesman, Max E.</creatorcontrib><creatorcontrib>Gautier, Jean</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Trends in biochemical sciences (Amsterdam. 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DNA interstrand crosslinks (ICLs) are complex lesions that block essential DNA transactions including DNA replication, recombination, and RNA transcription. Naturally occurring ICLs are rare, yet these lesions are the major cause of toxicity following treatment with several classes of crosslinking cancer chemotherapeutic drugs. ICLs are repaired during and outside of S phase by pathways with overlapping as well as distinct features. Here, we discuss some recent insights into the mechanisms of replication-dependent and replication-independent repair of ICLs with special emphasis on the differences between these repair pathways.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>23830640</pmid><doi>10.1016/j.tibs.2013.05.004</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antineoplastic Agents - adverse effects Cell Cycle Cross-Linking Reagents - adverse effects Cross-Linking Reagents - toxicity crosslinking DNA DNA Damage DNA Repair DNA Repair Enzymes - metabolism DNA replication drug therapy drugs Humans interphase Models, Biological Recombinational DNA Repair RNA S Phase toxicity |
title | The differences between ICL repair during and outside of S phase |
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