Uncoupling protein UCP2: When mitochondrial activity meets immunity

被引：107

作者：

Emre, Yalin ^{[2
]}

Nuebel, Tobias ^{[1
]}

机构：

[1] Deutsch Krebsforschungszentrum, German Canc Res Ctr, Div Signal Transduct & Growth Control, D-6900 Heidelberg, Germany

[2] Univ Geneva, Dept Pathol & Immunol, CMU, Geneva, Switzerland

来源：

FEBS LETTERS | 2010年 / 584卷 / 08期

关键词：

Mitochondria; Uncoupling protein 2; Reactive oxygen species; Inflammation; Immune response; BETA-CELL DYSFUNCTION; REACTIVE OXYGEN; MEDIATED INFLAMMATION; GLUTAMINE-METABOLISM; INSULIN-SECRETION; ROS PRODUCTION; NITRIC-OXIDE; FATTY-ACID; KAPPA-B; MACROPHAGES;

D O I：

10.1016/j.febslet.2010.03.014

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：

Uncoupling protein 2 (UCP2) belongs to the family of mitochondrial carriers. Here, we highlight recent findings regarding UCP2 function in the immune system. UCP2 controls immune cell activation by modulating MAPK pathways and the production of mitochondrial reactive oxygen species. In several models of infection, inflammation and autoimmunity, a regulatory impact of UCP2 was demonstrated by its direct implication in the production of cytokines and nitric oxide and in cell migration. In addition, UCP2 is reported as a key protein for oxidation of fatty acids, glutamine and glucose. Therefore we present a model of how the regulation of nutrient oxidation by UCP2 promotes immune cell activation. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：1437 / 1442

页数：6

共 64 条

[61] Stanniocalcin-1 suppresses superoxide generation in macrophages through induction of mitochondrial UCP2 [J].