The role of p38 MAP kinase in TGF-β1-induced signal transduction in human neutrophils

被引：102

作者：

Hannigan, M ^{[1
]}

Zhan, LJ ^{[1
]}

Ai, YX ^{[1
]}

Huang, CK ^{[1
]}

机构：

[1] Univ Connecticut, Ctr Hlth, Dept Pathol, Farmington, CT 06030 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1998年 / 246卷 / 01期

关键词：

D O I：

10.1006/bbrc.1998.8570

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Transforming growth factor-beta 1 (TGF-beta 1) is the strongest chemoattractant yet described for human neutrophils. It activates neither phospholipase C nor phospholipase D. It does not induce rises in intracellular calcium, degranulation, or superoxide production. The signaling pathways utilized by TGF-beta 1 are largely unknown. This report demonstrates that TGF-beta 1 activates p38 MAP kinase. The kinase inhibitor SB203580 blocks the chemotactic responses as well as actin polymerization induced by TGF-beta 1. Potential cellular targets of the p38 MAP kinase pathway which could mediate these function are discussed. (C) 1998 Academic Press.

引用

页码：55 / 58

页数：4

共 21 条

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