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rdf:type |
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lifeskim:mentions |
umls-concept:C0011155,
umls-concept:C0039194,
umls-concept:C0113519,
umls-concept:C0678226,
umls-concept:C0871261,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1719914,
umls-concept:C2349975,
umls-concept:C2828406,
umls-concept:C2911692
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pubmed:issue |
9
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pubmed:dateCreated |
2003-8-27
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pubmed:abstractText |
Much is known about how T cell receptor (TCR) engagement leads to T cell activation; however, the mechanisms terminating TCR signaling remain less clear. Diacylglycerol, generated after TCR ligation, is essential in T cells. Its function must be controlled tightly to maintain normal T cell homeostasis. Previous studies have shown that diacylglycerol kinase zeta (DGKzeta), which converts diacylglycerol to phosphatidic acid, can inhibit TCR signaling. Here we show that DGKzeta-deficient T cells are hyperresponsive to TCR stimulation both ex vivo and in vivo. Furthermore, DGKzeta-deficient mice mounted a more robust immune response to lymphocytic choriomeningitis virus infection than did wild-type mice. These results demonstrate the importance of DGKzeta as a physiological negative regulator of TCR signaling and T cell activation.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/CD69 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Diacylglycerol Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Guanine Nucleotide Exchange Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Rasgrp1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1529-2908
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
4
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
882-90
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:12883552-Animals,
pubmed-meshheading:12883552-Antigens, CD,
pubmed-meshheading:12883552-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:12883552-Cell Division,
pubmed-meshheading:12883552-DNA-Binding Proteins,
pubmed-meshheading:12883552-Diacylglycerol Kinase,
pubmed-meshheading:12883552-Flow Cytometry,
pubmed-meshheading:12883552-Guanine Nucleotide Exchange Factors,
pubmed-meshheading:12883552-Immunoblotting,
pubmed-meshheading:12883552-Lectins, C-Type,
pubmed-meshheading:12883552-Lymphocyte Activation,
pubmed-meshheading:12883552-Lymphocytic Choriomeningitis,
pubmed-meshheading:12883552-Mice,
pubmed-meshheading:12883552-Mice, Inbred C57BL,
pubmed-meshheading:12883552-Mice, Knockout,
pubmed-meshheading:12883552-Phosphatidic Acids,
pubmed-meshheading:12883552-Receptors, Antigen, T-Cell,
pubmed-meshheading:12883552-Receptors, Interleukin-2,
pubmed-meshheading:12883552-Signal Transduction,
pubmed-meshheading:12883552-T-Lymphocytes
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pubmed:year |
2003
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pubmed:articleTitle |
Enhanced T cell responses due to diacylglycerol kinase zeta deficiency.
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pubmed:affiliation |
The Signal Transduction Program, The Abramson Family Cancer Research Institute, Philadelphia, Pennsylvania 19104, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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