The ups and downs of MEK kinase interactions

被引：252

作者：

Hagemann, C ^{[1
]}

Blank, JL ^{[1
]}

机构：

[1] Univ Leicester, Dept Cell Physiol & Pharmacol, Leicester LE1 9HN, Leics, England

来源：

CELLULAR SIGNALLING | 2001年 / 13卷 / 12期

关键词：

MEKK; MEK kinase; stress-activated protein kinase cascade; JNK/SAPK; p38; protein-protein interactions; signal transduction; MEKK regulators; MEKK substrates;

D O I：

10.1016/S0898-6568(01)00220-0

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

MEK kinases (MEKKs) comprise a family of related serine-threonine protein kinases that regulate mitogen-activated protein kinase (MAPK) signalling pathways leading to c-Jun NH2-terminal kinase (JNK) and p38 activation, induced by cellular stress (e.g., UV and gamma irradiation, osmotic stress., heat shock, protein synthesis inhibitors), inflammatory cytokines (e.g., tumour necrosis factor alpha, TNF alpha and interleukin-1, IL1) and G protein-coupled receptor agonists (e.g., thrombin). These stress-activated kinases have been implicated in apoptosis, oncogenic transformation, and inflammatory responses in various cell types. At present, the signalling events involving MEKKs are not well understood. This review summarises our current knowledge concerning the regulation and function of MEKK family members, with particular emphasis on those factors capable of directly interacting with distinct MEKK isoforms. (C) 2001 Elsevier Science Inc. All rights reserved.

引用

页码：863 / 875

页数：13

共 109 条

[11]

2-1

[12] G alpha(12) stimulates c-Jun NH2-terminal kinase through the small G proteins Ras and Rac [J].

Collins, LR ;

Minden, A ;

Karin, M ;

Brown, JH .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (29) :17349-17353

[13] THE SMALL GTP-BINDING PROTEINS RAC1 AND CDC42 REGULATE THE ACTIVITY OF THE JNK/SAPK SIGNALING PATHWAY [J].

COSO, OA ;

CHIARIELLO, M ;

YU, JC ;

TERAMOTO, H ;

CRESPO, P ;

XU, NG ;

MIKI, T ;

GUTKIND, JS .

CELL, 1995, 81 (07) :1137-1146

[14] THE INS AND OUTS OF RAF KINASES [J].

DAUM, G ;

EISENMANNTAPPE, I ;

FRIES, HW ;

TROPPMAIR, J ;

RAPP, UR .

TRENDS IN BIOCHEMICAL SCIENCES, 1994, 19 (11) :474-480

[15] Signal transduction by the JNK group of MAP kinases [J].

Davis, RJ .

CELL, 2000, 103 (02) :239-252

[16] MEK kinase 3 directly activates MKK6 and MKK7, specific activators of the p38 and c-Jun NH2-terminal kinases [J].

Deacon, K ;

Blank, JL .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (23) :16604-16610

[17] Characterization of the mitogen-activated protein kinase kinase 4 (MKK4)/c-Jun NH2-terminal kinase 1 and MKK3/p38 pathways regulated by MEK kinases 2 and 3 - MEK kinase 3 activates MKK3 but does not cause activation of p38 kinase in vivo [J].

Deacon, K ;

Blank, JL .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (22) :14489-14496

[18] Fas-induced proteolytic activation and intracellular redistribution of the stress-signaling kinase MEKK1 [J].

Deak, JC ;

Cross, JV ;

Lewis, M ;

Qian, YY ;

Parrott, LA ;

Distelhorst, CW ;

Templeton, DJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (10) :5595-5600

[19] c-Jun inhibits transforming growth factor β-mediated transcription by repressing Smad3 transcriptional activity [J].

Dennler, S ;

Prunier, C ;

Ferrand, N ;

Gauthier, JM ;

Atfi, A .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (37) :28858-28865

[20] Activation of the c-Jun N-terminal kinase pathway by a novel protein kinase related to human germinal center kinase [J].

Diener, K ;

Wang, XHS ;

Chen, C ;

Meyer, CF ;

Keesler, G ;

Zukowski, M ;

Tan, TH ;

Yao, ZB .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (18) :9687-9692

← 1 2 3 4 5 6 7 8 9 10 →