LAT Is Required for TCR-Mediated Activation of PLC gamma 1 and the Ras Pathway
In this study, we present the further characterization of a mutant Jurkat T cell line, J.CaM2, that is defective in TCR-mediated signal transduction. Although initial TCR-mediated signaling events such as the inducible tyrosine phosphorylation of the TCR-\g?\ chain and ZAP-70 are intact in J.CaM2, s...
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Published in | Immunity (Cambridge, Mass.) Vol. 9; no. 5; pp. 617 - 626 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
01.11.1998
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Online Access | Get full text |
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Summary: | In this study, we present the further characterization of a mutant Jurkat T cell line, J.CaM2, that is defective in TCR-mediated signal transduction. Although initial TCR-mediated signaling events such as the inducible tyrosine phosphorylation of the TCR-\g?\ chain and ZAP-70 are intact in J.CaM2, subsequent events, including increases in intracellular calcium, Ras activation, and IL-2 gene expression are defective. Subsequent analysis of J.CaM2 demonstrated a severe deficiency in pp36/LAT expression, a recently cloned adaptor protein implicated in TCR signaling. Importantly, reexpression of LAT in J.CaM2 restored all aspects of TCR signaling. These results demonstrate a necessary and exclusive role for LAT in T cell activation. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 1074-7613 |
DOI: | 10.1016/S1074-7613(00)80659-7 |