TGF-β activates ERK5 in human renal epithelial cells

被引：11

作者：

Browne, James Alexander ^{[1
]}

Pearson, Alexander L. ^{[1
]}

Abou Zahr, Riad ^{[1
]}

Niculescu-Duvaz, Ioana ^{[1
]}

Baines, Deborah L. ^{[2
]}

Dockrell, Mark E. C. ^{[1
]}

机构：

[1] St Helier Hosp, S W Thames Inst Renal Res, Carshalton SM5 1AA, Surrey, England

[2] St Georges Univ London, London SW17 0RE, England

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2008年 / 373卷 / 03期

关键词：

extracellular signal-regulated kinase 5 (ERK5); TGF-beta; EGF; MAPK; PTEC; MEF2;

D O I：

10.1016/j.bbrc.2008.06.058

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：

The role of the MAP kinase, extracellular signal-regulated kinase 5 (ERK5) remains unknown, however it is involved in cell differentiation and survival as highlighted by the embryonic lethality of the ERK5 knockout. ERK5 can be activated by growth factors and other extracellular signals. TGF-beta, a powerful controller of epithelial cell phenotype, is known to activate the MAP kinase, ERK1/2 however its effect on ERK5 remains unknown. This study demonstrates, fort the first time, ERK5 activation by TGF-beta, observed in both transformed and primary adult human PTEC; activation required ALK-5 receptor activity. In addition this work demonstrates expression of myocyte enhancer factor-2 (MEF2C) by PTEC and that TGF-beta increased the association of MEK5 with phospho-ERK5 and MEF2C. ERK5 activation by either TGF-beta or epidermal growth factor (EGF) was also inhibited by the p38 MAP kinase inhibitor, SB-202190. (c) 2008 Elsevier Inc. All rights reserved.

引用

页码：440 / 444

页数：5

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