| pubmed-article:20661291 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20661291 | lifeskim:mentions | umls-concept:C0086411 | lld:lifeskim |
| pubmed-article:20661291 | lifeskim:mentions | umls-concept:C1708726 | lld:lifeskim |
| pubmed-article:20661291 | lifeskim:mentions | umls-concept:C0019646 | lld:lifeskim |
| pubmed-article:20661291 | lifeskim:mentions | umls-concept:C1415424 | lld:lifeskim |
| pubmed-article:20661291 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:20661291 | pubmed:dateCreated | 2010-7-27 | lld:pubmed |
| pubmed-article:20661291 | pubmed:abstractText | Somatic hypermutation introduces base substitutions into the rearranged and expressed immunoglobulin (Ig) variable regions to promote immunity. This pathway requires and is initiated by the Activation Induced Deaminase (AID) protein, which deaminates cytidine to produce uracils and UG mismatches at the Ig genes. Subsequent processing of uracil by mismatch repair and base excision repair factors contributes to mutagenesis. While selective for certain genomic targets, the chromatin modifications which distinguish hypermutating from non-hypermutating loci are not defined. | lld:pubmed |
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| pubmed-article:20661291 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:20661291 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20661291 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20661291 | pubmed:issn | 1932-6203 | lld:pubmed |
| pubmed-article:20661291 | pubmed:author | pubmed-author:LarsonErik... | lld:pubmed |
| pubmed-article:20661291 | pubmed:author | pubmed-author:VogelLaura... | lld:pubmed |
| pubmed-article:20661291 | pubmed:author | pubmed-author:EdwardsKevin... | lld:pubmed |
| pubmed-article:20661291 | pubmed:author | pubmed-author:BorchertGlen... | lld:pubmed |
| pubmed-article:20661291 | pubmed:author | pubmed-author:HoltonNathani... | lld:pubmed |
| pubmed-article:20661291 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20661291 | pubmed:volume | 5 | lld:pubmed |
| pubmed-article:20661291 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20661291 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20661291 | pubmed:pagination | e11641 | lld:pubmed |
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| pubmed-article:20661291 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20661291 | pubmed:articleTitle | Histone H2A and H2B are monoubiquitinated at AID-targeted loci. | lld:pubmed |
| pubmed-article:20661291 | pubmed:affiliation | School of Biological Sciences, Illinois State University, Normal, Illinois, United States of America. | lld:pubmed |
| pubmed-article:20661291 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20661291 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:20661291 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
