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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2009-11-16
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pubmed:abstractText |
The survival of T lymphocytes requires sustained, Ca(2+) influx-dependent gene expression. The molecular mechanism that governs sustained Ca(2+) influx in naive T lymphocytes is unknown. Here we report an essential role for the beta3 regulatory subunit of voltage-gated calcium (Ca(v)) channels in the maintenance of naive CD8(+) T cells. Deficiency in beta3 resulted in a profound survival defect of CD8(+) T cells. This defect correlated with depletion of the pore-forming subunit Ca(v)1.4 and attenuation of T cell antigen receptor (TCR)-mediated global Ca(2+) entry in CD8(+) T cells. Ca(v)1.4 and beta3 associated with T cell signaling machinery and Ca(v)1.4 localized in lipid rafts. Our data demonstrate a mechanism by which Ca(2+) entry is controlled by a Ca(v)1.4-beta3 channel complex in T cells.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19838200-10037236,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19838200-10494839,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/19838200-12838335,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/19838200-19318619,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19838200-19324409,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19838200-9050842,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/19838200-9890976
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1529-2916
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1275-82
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pubmed:dateRevised |
2010-9-27
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pubmed:meshHeading |
pubmed-meshheading:19838200-Animals,
pubmed-meshheading:19838200-Antigens, CD95,
pubmed-meshheading:19838200-Apoptosis,
pubmed-meshheading:19838200-CD8-Positive T-Lymphocytes,
pubmed-meshheading:19838200-Calcium Channels,
pubmed-meshheading:19838200-Calcium Signaling,
pubmed-meshheading:19838200-Cell Survival,
pubmed-meshheading:19838200-Gene Expression Regulation,
pubmed-meshheading:19838200-Homeostasis,
pubmed-meshheading:19838200-Immunity, Innate,
pubmed-meshheading:19838200-Mice,
pubmed-meshheading:19838200-Mice, Knockout
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pubmed:year |
2009
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pubmed:articleTitle |
Defective survival of naive CD8+ T lymphocytes in the absence of the beta3 regulatory subunit of voltage-gated calcium channels.
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pubmed:affiliation |
Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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