pubmed-article:16309779 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16309779 | lifeskim:mentions | umls-concept:C0034865 | lld:lifeskim |
pubmed-article:16309779 | lifeskim:mentions | umls-concept:C0003241 | lld:lifeskim |
pubmed-article:16309779 | lifeskim:mentions | umls-concept:C1155661 | lld:lifeskim |
pubmed-article:16309779 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:16309779 | pubmed:dateCreated | 2006-1-2 | lld:pubmed |
pubmed-article:16309779 | pubmed:abstractText | Mismatch repair (MMR) proteins are important for antibody class-switch recombination (CSR), but their roles are unknown. We propose a model for the function of MMR in CSR in which MMR proteins convert single-strand nicks instigated by activation-induced cytidine deaminase (AID) into the double-strand breaks (DSBs) that are required for CSR. This model does not invoke any novel functions for MMR but simply posits that, owing to numerous single-strand nicks in the switch (S) regions of both DNA strands, when MMR proteins are recruited by U:G mismatches, they excise one strand of DNA and soon reach a nick on the opposite strand. This halts excision activity and creates a DSB. This model explains why B cells that lack either S mu and MSH2 or UNG and MSH2 cannot undergo CSR. | lld:pubmed |
pubmed-article:16309779 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16309779 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16309779 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16309779 | pubmed:language | eng | lld:pubmed |
pubmed-article:16309779 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16309779 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16309779 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16309779 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16309779 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16309779 | pubmed:month | Jan | lld:pubmed |
pubmed-article:16309779 | pubmed:issn | 0168-9525 | lld:pubmed |
pubmed-article:16309779 | pubmed:author | pubmed-author:SchraderCarol... | lld:pubmed |
pubmed-article:16309779 | pubmed:author | pubmed-author:StavnezerJane... | lld:pubmed |
pubmed-article:16309779 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16309779 | pubmed:volume | 22 | lld:pubmed |
pubmed-article:16309779 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16309779 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16309779 | pubmed:pagination | 23-8 | lld:pubmed |
pubmed-article:16309779 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
pubmed-article:16309779 | pubmed:meshHeading | pubmed-meshheading:16309779... | lld:pubmed |
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pubmed-article:16309779 | pubmed:meshHeading | pubmed-meshheading:16309779... | lld:pubmed |
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pubmed-article:16309779 | pubmed:meshHeading | pubmed-meshheading:16309779... | lld:pubmed |
pubmed-article:16309779 | pubmed:meshHeading | pubmed-meshheading:16309779... | lld:pubmed |
pubmed-article:16309779 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16309779 | pubmed:articleTitle | Mismatch repair converts AID-instigated nicks to double-strand breaks for antibody class-switch recombination. | lld:pubmed |
pubmed-article:16309779 | pubmed:affiliation | Department of Molecular Genetics and Microbiology, Program in Immunology and Virology, University of Massachusetts Medical School, Worcester, MA 01655-0122, USA. janet.stavnezer@umassmed.edu | lld:pubmed |
pubmed-article:16309779 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16309779 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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