[HTML][HTML] LAT is required for TCR-mediated activation of PLCγ1 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-ζ 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 …
that is defective in TCR-mediated signal transduction. Although initial TCR-mediated
signaling events such as the inducible tyrosine phosphorylation of the TCR-ζ 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 …
Abstract
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-ζ 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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