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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2010-9-3
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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.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD45,
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins,
http://linkedlifedata.com/resource/pubmed/chemical/NFATC Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Nfatc1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Ptprc protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/RAG-1 protein,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, B-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Siglec-G protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1550-6606
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
185
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3277-84
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pubmed:meshHeading |
pubmed-meshheading:20729333-Adoptive Transfer,
pubmed-meshheading:20729333-Animals,
pubmed-meshheading:20729333-Antigens, CD45,
pubmed-meshheading:20729333-B-Lymphocyte Subsets,
pubmed-meshheading:20729333-Cell Compartmentation,
pubmed-meshheading:20729333-Cell Proliferation,
pubmed-meshheading:20729333-Cell Survival,
pubmed-meshheading:20729333-Cells, Cultured,
pubmed-meshheading:20729333-Homeodomain Proteins,
pubmed-meshheading:20729333-Lectins,
pubmed-meshheading:20729333-Lymphocyte Activation,
pubmed-meshheading:20729333-Mice,
pubmed-meshheading:20729333-Mice, Inbred BALB C,
pubmed-meshheading:20729333-Mice, Knockout,
pubmed-meshheading:20729333-NFATC Transcription Factors,
pubmed-meshheading:20729333-Peritoneum,
pubmed-meshheading:20729333-Receptors, Antigen, B-Cell,
pubmed-meshheading:20729333-Up-Regulation
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pubmed:year |
2010
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pubmed:articleTitle |
Siglec-G regulates B1 cell survival and selection.
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pubmed:affiliation |
Department of Genetics, University of Erlangen, Erlangen, Germany.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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