The role of p38 MAP kinase in TGF-β1-induced signal transduction in human neutrophils
The role of p38 MAP kinase in TGF-β1-induced signal transduction in human neutrophils
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DOI：
10.1006/bbrc.1998.8570
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发表时间：
1998-05-08
影响因子：
3.1
通讯作者：
Huang, CK
中科院分区：
文献类型：
--
作者：
Hannigan, M;Zhan, LJ;Huang, CK
转化生长因子-β 1 (TGF-β 1) 是迄今为止对人类中性粒细胞最强的化学引诱剂。它既不激活磷脂酶 C 也不激活磷脂酶 D。它不会引起细胞内钙的增加、脱颗粒或超氧化物的产生。 TGF-β1 利用的信号传导途径很大程度上未知。该报告表明 TGF-β 1 激活 p38 MAP 激酶。激酶抑制剂 SB203580 可阻断 TGF-β 1 诱导的趋化反应以及肌动蛋白聚合。讨论了可介导这些功能的 p38 MAP 激酶途径的潜在细胞靶标。 (C) 1998 年学术出版社。
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.