MAPK signalling in cellular metabolism: stress or wellness?

被引：234

作者：

Gehart, Helmuth ^{[2
]}

Kumpf, Susann

Ittner, Arne ^{[2
]}

Ricci, Romeo ^{[1
,2
,3
]}

机构：

[1] ETH, Inst Cell Biol, Dept Biol, CH-8093 Zurich, Switzerland

[2] CNRS INSERM ULP, IGMBC, F-67404 Illkirch Graffenstaden, France

[3] Hop Univ Strasbourg, Serv Biochim & Biol Mol, Strasbourg, France

来源：

EMBO REPORTS | 2010年 / 11卷 / 11期

关键词：

diabetes; insulin signalling; MAPK; metabolism; obesity; ACTIVATED PROTEIN-KINASE; N-TERMINAL KINASE; ENDOPLASMIC-RETICULUM STRESS; GLYCOGEN-SYNTHASE KINASE-3; GLUCOCORTICOID-RECEPTOR; INSULIN-RESISTANCE; IN-VIVO; ADIPOCYTE DIFFERENTIATION; MEDIATED PHOSPHORYLATION; GLUCOSE-HOMEOSTASIS;

D O I：

10.1038/embor.2010.160

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：

Mitogen-activated protein kinase (MAPK) signalling occurs in response to almost any change in the extracellular or intra-cellular milieu that affects the metabolism of the cell, organ or the entire organism. MAPK-dependent signal transduction is required for physiological metabolic adaptation, but inappropriate MAPK signalling contributes to the development of several interdependent pathological traits, collectively known as metabolic syndrome. Metabolic syndrome leads to life-threatening clinical consequences, such as type 2 diabetes. This Review provides an overview of the MAPK-signalling mechanisms that underly basic cellular metabolism, discussing their link to disease.

引用

页码：834 / 840

页数：7

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