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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0039194,
umls-concept:C0185117,
umls-concept:C0205263,
umls-concept:C0812215,
umls-concept:C1413235,
umls-concept:C1527180,
umls-concept:C1548966,
umls-concept:C1706586,
umls-concept:C1710082,
umls-concept:C1999230,
umls-concept:C2746015,
umls-concept:C2911684
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pubmed:issue |
12
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pubmed:dateCreated |
1996-3-1
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pubmed:abstractText |
Stimulation of the T cell antigen receptor (TCR) induces a number of intracellular signaling pathways which lead to the transcription of a variety of new genes. Of the newly synthesized proteins, the earliest to be detected on the cell surface is the type II integral membrane protein CD69. Cross-linking of this activation antigen induces signaling events related to T cell activation. The proto-oncogene product Ras has been reported to up-regulate CD69. However, which of the potential effectors of Ras induces the expression of CD69 has remained unclear. Using transient transfection, we have shown a constitutively active form of the serine/threonine kinase Raf-1 to be sufficient to induce CD69 expression in human Jurkat T cells. Raf-1 was further shown to be necessary for PMA-induced CD69 expression, since transfection of a dominant inhibitory form of Raf-1 blocked the up-regulation of CD69 by PMA. In addition, studies with the calcium ionophore ionomycin identified a previously uncharacterized pathway regulating the expression of CD69 in T cells. Elevation of intracellular calcium induced the expression of CD69 in both Jurkat cells and peripheral blood T cells. This effect was sensitive to the immunosuppressive drug cyclosporin A, indicating that calcium-induced CD69 expression is mediated by the protein phosphatase calcineurin. Taken together, these results define Raf-1 as the major signaling mediator of CD69 expression in T cells and suggest that multiple mechanisms exist to regulate the level of CD69 expression following TCR stimulation.
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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/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Ionomycin,
http://linkedlifedata.com/resource/pubmed/chemical/Ionophores,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogens,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-raf,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0014-2980
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3215-21
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:8566003-Antigens, CD,
pubmed-meshheading:8566003-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:8566003-Cyclosporine,
pubmed-meshheading:8566003-Dose-Response Relationship, Immunologic,
pubmed-meshheading:8566003-Down-Regulation,
pubmed-meshheading:8566003-Humans,
pubmed-meshheading:8566003-Immunosuppressive Agents,
pubmed-meshheading:8566003-Ionomycin,
pubmed-meshheading:8566003-Ionophores,
pubmed-meshheading:8566003-Lectins, C-Type,
pubmed-meshheading:8566003-Lymphoma,
pubmed-meshheading:8566003-Mitogens,
pubmed-meshheading:8566003-Protein-Serine-Threonine Kinases,
pubmed-meshheading:8566003-Proto-Oncogene Proteins,
pubmed-meshheading:8566003-Proto-Oncogene Proteins c-raf,
pubmed-meshheading:8566003-Signal Transduction,
pubmed-meshheading:8566003-T-Lymphocytes,
pubmed-meshheading:8566003-Tetradecanoylphorbol Acetate,
pubmed-meshheading:8566003-Tumor Cells, Cultured,
pubmed-meshheading:8566003-Up-Regulation
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pubmed:year |
1995
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pubmed:articleTitle |
Raf-1 provides a dominant but not exclusive signal for the induction of CD69 expression on T cells.
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pubmed:affiliation |
Signal Transduction Branch, Naval Medical Research Institute, Bethesda, MD 20889, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.
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