| pubmed-article:15860226 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15860226 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:15860226 | lifeskim:mentions | umls-concept:C0205307 | lld:lifeskim |
| pubmed-article:15860226 | lifeskim:mentions | umls-concept:C0017350 | lld:lifeskim |
| pubmed-article:15860226 | lifeskim:mentions | umls-concept:C0443009 | lld:lifeskim |
| pubmed-article:15860226 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15860226 | pubmed:dateCreated | 2005-4-29 | lld:pubmed |
| pubmed-article:15860226 | pubmed:abstractText | Somatic hypermutation (SHM) occurs in the variable region of immunoglobulin genes in germinal center B cells where it plays an important role in affinity maturation of the T cell-dependent immune response. Although the precise mechanism of SHM is still unknown, it has been suggested that error-prone DNA polymerases (Pol) are involved in SHM. Poliota is a member of the error-prone Y-family of DNA polymerases which exhibit translesion synthesis activity in vitro and are highly mutagenic when replicating on non-damaged DNA templates. In BL2 cell line stimulated to induce SHM, the induction is Poliota-dependent. However, in 129-derived strains of mice deficient in Poliota, SHM is normal. One possible explanation for this discrepancy is that a Poliota deficiency in mice might be compensated for by another error-prone DNA polymerase, such as Polkappa, which also belongs to the Y-family of DNA polymerases. Although SHM in Polkappa-deficient mice is normal, their deficiency might be compensated for by Poliota. In this study, we generated Polkappa-Poliota double-deficient mice and examined them for SHM. We found that the double-deficient mice had the normal SHM frequency and profile, rendering them indistinguishable from Polkappa-deficient mice and thus conclude that Poliota and Polkappa are dispensable for SHM in mice. | lld:pubmed |
| pubmed-article:15860226 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15860226 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15860226 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15860226 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15860226 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15860226 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15860226 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15860226 | pubmed:month | May | lld:pubmed |
| pubmed-article:15860226 | pubmed:issn | 0165-2478 | lld:pubmed |
| pubmed-article:15860226 | pubmed:author | pubmed-author:OhmoriHaruoH | lld:pubmed |
| pubmed-article:15860226 | pubmed:author | pubmed-author:ShimizuTakeyu... | lld:pubmed |
| pubmed-article:15860226 | pubmed:author | pubmed-author:YamadaShuichi... | lld:pubmed |
| pubmed-article:15860226 | pubmed:author | pubmed-author:AzumaTakachik... | lld:pubmed |
| pubmed-article:15860226 | pubmed:author | pubmed-author:KanjoNaokoN | lld:pubmed |
| pubmed-article:15860226 | pubmed:author | pubmed-author:IshiguroMarik... | lld:pubmed |
| pubmed-article:15860226 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15860226 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:15860226 | pubmed:volume | 98 | lld:pubmed |
| pubmed-article:15860226 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15860226 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15860226 | pubmed:pagination | 259-64 | lld:pubmed |
| pubmed-article:15860226 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:15860226 | pubmed:meshHeading | pubmed-meshheading:15860226... | lld:pubmed |
| pubmed-article:15860226 | pubmed:meshHeading | pubmed-meshheading:15860226... | lld:pubmed |
| pubmed-article:15860226 | pubmed:meshHeading | pubmed-meshheading:15860226... | lld:pubmed |
| pubmed-article:15860226 | pubmed:meshHeading | pubmed-meshheading:15860226... | lld:pubmed |
| pubmed-article:15860226 | pubmed:meshHeading | pubmed-meshheading:15860226... | lld:pubmed |
| pubmed-article:15860226 | pubmed:meshHeading | pubmed-meshheading:15860226... | lld:pubmed |
| pubmed-article:15860226 | pubmed:meshHeading | pubmed-meshheading:15860226... | lld:pubmed |
| pubmed-article:15860226 | pubmed:meshHeading | pubmed-meshheading:15860226... | lld:pubmed |
| pubmed-article:15860226 | pubmed:meshHeading | pubmed-meshheading:15860226... | lld:pubmed |
| pubmed-article:15860226 | pubmed:meshHeading | pubmed-meshheading:15860226... | lld:pubmed |
| pubmed-article:15860226 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15860226 | pubmed:articleTitle | Normal immunoglobulin gene somatic hypermutation in Pol kappa-Pol iota double-deficient mice. | lld:pubmed |
| pubmed-article:15860226 | pubmed:affiliation | Division of Biosignaling, Research Institute for Biological Sciences (RIBS), Tokyo University of Science, Yamazaki 2669, Noda, Chiba 278-0022, Japan. | lld:pubmed |
| pubmed-article:15860226 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15860226 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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