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...

Full description

Saved in:
Bibliographic Details
Published inImmunity (Cambridge, Mass.) Vol. 9; no. 5; pp. 617 - 626
Main Authors Finco, T S, Kadlecek, T, Zhang, W, Samelson, LE, Weiss, A
Format Journal Article
LanguageEnglish
Published 01.11.1998
Online AccessGet full text

Cover

Loading…
More Information
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.
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