Activation of Pyk2 by stress signals and coupling with JNK signaling pathway.

Article Details

Citation

Tokiwa G, Dikic I, Lev S, Schlessinger J

Activation of Pyk2 by stress signals and coupling with JNK signaling pathway.

Science. 1996 Aug 9;273(5276):792-4.

PubMed ID
8670418 [ View in PubMed
]
Abstract

The c-Jun amino-terminal kinase (JNK) is activated by various heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptors, inflammatory cytokines, and stress signals. Yet, upstream mediators that link extracellular signals with the JNK signaling pathway are currently unknown. The tyrosine kinase Pyk2 was activated by tumor necrosis factor alpha, by ultraviolet irradiation, and by changes in osmolarity. Overexpression of Pyk2 led to activation of JNK, and a dominant-negative mutant of Pyk2 interfered with ultraviolet light- or osmotic shock-induced activation of JNK. Pyk2 represents a cell type-specific, stress-sensitive mediator of the JNK signaling pathway.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Protein-tyrosine kinase 2-betaQ14289Details