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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5960
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pubmed:dateCreated |
2009-12-18
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pubmed:databankReference |
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pubmed:abstractText |
Fanconi anemia is a human cancer predisposition syndrome caused by mutations in 13 Fanc genes. The disorder is characterized by genomic instability and cellular hypersensitivity to chemicals that generate DNA interstrand cross-links (ICLs). A central event in the activation of the Fanconi anemia pathway is the mono-ubiquitylation of the FANCI-FANCD2 complex, but how this complex confers ICL resistance remains enigmatic. Using a cell-free system, we showed that FANCI-FANCD2 is required for replication-coupled ICL repair in S phase. Removal of FANCD2 from extracts inhibits both nucleolytic incisions near the ICL and translesion DNA synthesis past the lesion. Reversal of these defects requires ubiquitylated FANCI-FANCD2. Our results show that multiple steps of the essential S-phase ICL repair mechanism fail when the Fanconi anemia pathway is compromised.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-11239454,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-11749045,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-12065746,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-12239151,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-12509764,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-15199141,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-15327776,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-16382135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-17412408,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-17481966,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-17768402,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-18448394,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-18805090,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-18931676,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-19111657,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-19596231,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-19748363,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19965384-19748364
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1095-9203
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
18
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pubmed:volume |
326
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1698-701
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pubmed:dateRevised |
2011-9-26
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pubmed:meshHeading |
pubmed-meshheading:19965384-Animals,
pubmed-meshheading:19965384-Cell-Free System,
pubmed-meshheading:19965384-Chromatin,
pubmed-meshheading:19965384-DNA,
pubmed-meshheading:19965384-DNA Damage,
pubmed-meshheading:19965384-DNA Repair,
pubmed-meshheading:19965384-DNA Replication,
pubmed-meshheading:19965384-Fanconi Anemia,
pubmed-meshheading:19965384-Fanconi Anemia Complementation Group D2 Protein,
pubmed-meshheading:19965384-Fanconi Anemia Complementation Group Proteins,
pubmed-meshheading:19965384-Molecular Sequence Data,
pubmed-meshheading:19965384-Recombinant Proteins,
pubmed-meshheading:19965384-S Phase,
pubmed-meshheading:19965384-Signal Transduction,
pubmed-meshheading:19965384-Ubiquitinated Proteins,
pubmed-meshheading:19965384-Ubiquitination,
pubmed-meshheading:19965384-Xenopus Proteins,
pubmed-meshheading:19965384-Xenopus laevis
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pubmed:year |
2009
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pubmed:articleTitle |
The Fanconi anemia pathway promotes replication-dependent DNA interstrand cross-link repair.
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pubmed:affiliation |
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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