| pubmed-article:19633670 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19633670 | lifeskim:mentions | umls-concept:C0021017 | lld:lifeskim |
| pubmed-article:19633670 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:19633670 | lifeskim:mentions | umls-concept:C0206071 | lld:lifeskim |
| pubmed-article:19633670 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:19633670 | lifeskim:mentions | umls-concept:C0439064 | lld:lifeskim |
| pubmed-article:19633670 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:19633670 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:19633670 | pubmed:dateCreated | 2009-8-5 | lld:pubmed |
| pubmed-article:19633670 | pubmed:abstractText | The Mre11-Rad50-NBS1 (MRN) complex has many roles in response to DNA double-strand breaks, but its functions in repair by nonhomologous end joining (NHEJ) pathways are poorly understood. We have investigated requirements for MRN in class switch recombination (CSR), a programmed DNA rearrangement in B lymphocytes that requires NHEJ. To this end, we have engineered mice that lack the entire MRN complex in B lymphocytes or that possess an intact complex that harbors mutant Mre11 lacking DNA nuclease activities. MRN deficiency confers a strong defect in CSR, affecting both the classic and the alternative NHEJ pathways. In contrast, absence of Mre11 nuclease activities causes a milder phenotype, revealing a separation of function within the complex. We propose a model in which MRN stabilizes distant breaks and processes DNA termini to facilitate repair by both the classical and alternative NHEJ pathways. | lld:pubmed |
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| pubmed-article:19633670 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19633670 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19633670 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19633670 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19633670 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:19633670 | pubmed:issn | 1545-9985 | lld:pubmed |
| pubmed-article:19633670 | pubmed:author | pubmed-author:FergusonDavid... | lld:pubmed |
| pubmed-article:19633670 | pubmed:author | pubmed-author:SekiguchiJoAn... | lld:pubmed |
| pubmed-article:19633670 | pubmed:author | pubmed-author:WuYipinY | lld:pubmed |
| pubmed-article:19633670 | pubmed:author | pubmed-author:BuisJeffreyJ | lld:pubmed |
| pubmed-article:19633670 | pubmed:author | pubmed-author:DinkelmannMar... | lld:pubmed |
| pubmed-article:19633670 | pubmed:author | pubmed-author:SpehalskiEliz... | lld:pubmed |
| pubmed-article:19633670 | pubmed:author | pubmed-author:StonehamTrina... | lld:pubmed |
| pubmed-article:19633670 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19633670 | pubmed:volume | 16 | lld:pubmed |
