pubmed-article:17142237 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17142237 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:17142237 | lifeskim:mentions | umls-concept:C0205103 | lld:lifeskim |
pubmed-article:17142237 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
pubmed-article:17142237 | lifeskim:mentions | umls-concept:C0017350 | lld:lifeskim |
pubmed-article:17142237 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
pubmed-article:17142237 | lifeskim:mentions | umls-concept:C1979882 | lld:lifeskim |
pubmed-article:17142237 | lifeskim:mentions | umls-concept:C0017259 | lld:lifeskim |
pubmed-article:17142237 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:17142237 | pubmed:issue | 21 | lld:pubmed |
pubmed-article:17142237 | pubmed:dateCreated | 2006-12-6 | lld:pubmed |
pubmed-article:17142237 | pubmed:abstractText | Activation-induced cytidine deaminase (AID) likely initiates immunoglobulin gene-conversion (GC) by deaminating cytidines within the V-region of chicken B-cells. However, the intervening DNA lesion required to initiate GC remains elusive. GC could be initiated by a single strand break or a double strand break (DSB). To distinguish between these possibilities, we examined GC in the chicken DT40 B cell line deficient in non-homologous end joining (NHEJ). It is known that the NHEJ and homologous recombination DNA repair pathways compete for DSBs. In light of this, if a DSB is the major intermediate, deficiency in NHEJ should result in increased levels of GC. Here we show that DNA-PKcs(-/-/-) and Ku70(-/-) DT40 cells had 5- to 10-fold higher levels of GC relative to wildtype DT40 as measured by surface IgM reversion and sequencing of the V-region. These data suggest that a DSB is the major DNA lesion that initiates GC. | lld:pubmed |
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pubmed-article:17142237 | pubmed:language | eng | lld:pubmed |
pubmed-article:17142237 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17142237 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17142237 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17142237 | pubmed:issn | 1362-4962 | lld:pubmed |
pubmed-article:17142237 | pubmed:author | pubmed-author:MartinAlberto... | lld:pubmed |
pubmed-article:17142237 | pubmed:author | pubmed-author:TangEphraim... | lld:pubmed |
pubmed-article:17142237 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:17142237 | pubmed:volume | 34 | lld:pubmed |
pubmed-article:17142237 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17142237 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17142237 | pubmed:pagination | 6345-51 | lld:pubmed |
pubmed-article:17142237 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:17142237 | pubmed:meshHeading | pubmed-meshheading:17142237... | lld:pubmed |
pubmed-article:17142237 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:17142237 | pubmed:articleTitle | NHEJ-deficient DT40 cells have increased levels of immunoglobulin gene conversion: evidence for a double strand break intermediate. | lld:pubmed |
pubmed-article:17142237 | pubmed:affiliation | Department of Immunology, 5265 Medical Sciences Building, University of Toronto, Ontario, Toronto, Canada M5S 1A8. | lld:pubmed |
pubmed-article:17142237 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17142237 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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