当前位置： SCI文献检索 > BIOCHEMISTRY期刊下所有文献 > Differential regulation of oxidative and osmotic stress induced Syk activation by both autophosphorylation and SH2 domains.

Differential regulation of oxidative and osmotic stress induced Syk activation by both autophosphorylation and SH2 domains.

Abstract：

:Syk, a nonreceptor protein-tyrosine kinase, is activated by both oxidative and osmotic stress and plays different roles in the transduction of stress signals. In this study, the regulation of oxidative and osmotic stress induced Syk activation was investigated utilizing Syk-negative DT40 cells, expressing various Syk mutants. Phosphorylation of Y518Y519 was demonstrated to be required for both oxidative and osmotic stress induced Syk activation. Syk activation by these two types of stress stimuli was a combination of both autophosphorylation and the activities of additional tyrosine kinases. Oxidative stress induced Syk tyrosine phosphorylation was almost completely attributed to autophosphorylation, whereas other tyrosine kinases were largely responsible for osmotic stress induced Syk tyrosine phosphorylation. Moreover, the Src homology 2 (SH2) domains of Syk differentially regulated Syk activation. Both mSH2(N) Syk and mSH2(C) Syk, in which the phosphotyrosine-dependent binding motif within the SH2 domains contained point mutations, showed a significantly higher activity than that observed in wild-type Syk, following osmotic stress treatment. In comparison, in response to oxidative stress, only mSH2(N) Syk demonstrated a stronger activation than wild-type Syk. Therefore, differential activation and regulation of Syk may give an insight into the distinctive functions of Syk in oxidative and osmotic stress signaling.

journal_name

Biochemistry

journal_title

Biochemistry

authors

Qin S,Kurosaki T,Yamamura H

doi

10.1021/bi9729460

subject

Has Abstract

pub_date

1998-04-21 00:00:00

pages

5481-6

issue

16

eissn

0006-2960

issn

1520-4995

pii

bi9729460

journal_volume

37

pub_type

杂志文章

相关文献

BIOCHEMISTRY文献大全