| pubmed-article:20729333 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20729333 | lifeskim:mentions | umls-concept:C0007620 | lld:lifeskim |
| pubmed-article:20729333 | lifeskim:mentions | umls-concept:C0036576 | lld:lifeskim |
| pubmed-article:20729333 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:20729333 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:20729333 | pubmed:dateCreated | 2010-9-3 | lld:pubmed |
| pubmed-article:20729333 | pubmed:abstractText | Siglec-G is a negative regulator of BCR-mediated signaling in B1a cells. This population of B cells is highly increased in Siglec-G-deficient mice, but the mechanism of this expansion is not known so far. In this study, we demonstrate that Siglecg(-/-) B1a cells show a lower level of spontaneous apoptosis and a prolonged life span. Mechanistically, the lower apoptosis could result from higher expression levels of the transcription factor NFATc1 in Siglec-G-deficient B1a cells. Interestingly, Siglecg(-/-) B1a cells display an altered BCR repertoire compared with wild-type B1a cells. As the BCR repertoire and the VDJ composition of Igs of Siglecg(-/-) B1a cells resembles more the Abs produced by adult bone marrow-derived B cells rather than canonical fetal liver-derived B1a cells, this suggest that the selection into the B1a cell population is altered in Siglec-G-deficient mice. | lld:pubmed |
| pubmed-article:20729333 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20729333 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20729333 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:20729333 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20729333 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20729333 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20729333 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20729333 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20729333 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:20729333 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:20729333 | pubmed:author | pubmed-author:NitschkeLarsL | lld:pubmed |
| pubmed-article:20729333 | pubmed:author | pubmed-author:WeissSiegfrie... | lld:pubmed |
| pubmed-article:20729333 | pubmed:author | pubmed-author:BinderChristo... | lld:pubmed |
| pubmed-article:20729333 | pubmed:author | pubmed-author:VollReinhardR | lld:pubmed |
| pubmed-article:20729333 | pubmed:author | pubmed-author:DüberSandraS | lld:pubmed |
| pubmed-article:20729333 | pubmed:author | pubmed-author:GückelEvaE | lld:pubmed |
| pubmed-article:20729333 | pubmed:author | pubmed-author:JellusovaJuli... | lld:pubmed |
| pubmed-article:20729333 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20729333 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:20729333 | pubmed:volume | 185 | lld:pubmed |
| pubmed-article:20729333 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20729333 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20729333 | pubmed:pagination | 3277-84 | lld:pubmed |
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| pubmed-article:20729333 | pubmed:meshHeading | pubmed-meshheading:20729333... | lld:pubmed |
| pubmed-article:20729333 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20729333 | pubmed:articleTitle | Siglec-G regulates B1 cell survival and selection. | lld:pubmed |
| pubmed-article:20729333 | pubmed:affiliation | Department of Genetics, University of Erlangen, Erlangen, Germany. | lld:pubmed |
| pubmed-article:20729333 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20729333 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:20729333 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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