Document Detail

The regulation and turnover of mitochondrial uncoupling proteins.
MedLine Citation:
PMID:  20211596     Owner:  NLM     Status:  MEDLINE    
Uncoupling proteins (UCP1, UCP2 and UCP3) are important in regulating cellular fuel metabolism and as attenuators of reactive oxygen species production through strong or mild uncoupling. The generic function and broad tissue distribution of the uncoupling protein family means that they are increasingly implicated in a range of pathophysiological processes including obesity, insulin resistance and diabetes mellitus, neurodegeneration, cardiovascular disease, immunity and cancer. The significant recent progress describing the turnover of novel uncoupling proteins, as well as current views on the physiological roles and regulation of UCPs, is outlined.
Vian Azzu; Martin Jastroch; Ajit S Divakaruni; Martin D Brand
Related Documents :
16520066 - Mitochondrial proteomic characterization of human normal articular chondrocytes.
18219256 - Mortalin: a protein associated with progression of parkinson disease?
20675386 - Stabilization of hypoxia-inducible factor-1alpha protein in hypoxia occurs independentl...
17002876 - Differential efflux of mitochondrial endonuclease g by hnoxa and tbid.
19258536 - Pivotal roles of the outer membrane polysaccharide export and polysaccharide copolymera...
22124706 - Differential protein expression in tears of patients with primary open angle and pseudo...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2010-03-06
Journal Detail:
Title:  Biochimica et biophysica acta     Volume:  1797     ISSN:  0006-3002     ISO Abbreviation:  Biochim. Biophys. Acta     Publication Date:    2010 Jun-Jul
Date Detail:
Created Date:  2010-06-21     Completed Date:  2011-01-10     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  0217513     Medline TA:  Biochim Biophys Acta     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  785-91     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier B.V. All rights reserved.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Diabetes Mellitus / metabolism
Energy Metabolism
Gene Expression
Insulin Resistance
Ion Channels / genetics,  metabolism*
Mitochondria / metabolism
Mitochondrial Proteins / genetics,  metabolism*
Models, Biological
Obesity / metabolism
Grant Support
MC_U105663137//Medical Research Council; P01 AG025901/AG/NIA NIH HHS; P01 AG025901/AG/NIA NIH HHS; P01 AG025901-03/AG/NIA NIH HHS; P01 AG025901-04/AG/NIA NIH HHS; P30 AG025708/AG/NIA NIH HHS; P30 AG025708/AG/NIA NIH HHS; P30 AG025708-04/AG/NIA NIH HHS; P30 AG025708-05/AG/NIA NIH HHS; PL1 AG032118/AG/NIA NIH HHS; R01 AG033542/AG/NIA NIH HHS; R01 AG033542/AG/NIA NIH HHS; R01 AG033542-01/AG/NIA NIH HHS; UL1 DE019608/DE/NIDCR NIH HHS; UL1 DE019608-02/DE/NIDCR NIH HHS; UL1 DE019608-02S1/DE/NIDCR NIH HHS; UL1 DE019608-03/DE/NIDCR NIH HHS; //Medical Research Council
Reg. No./Substance:
0/Ion Channels; 0/Mitochondrial Proteins; 0/mitochondrial uncoupling protein; 0/mitochondrial uncoupling protein 2; 0/mitochondrial uncoupling protein 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Plasticity of the mitoproteome to nitrogen sources (nitrate and ammonium) in Chlamydomonas reinhardt...
Next Document:  Human mitochondrial mRNAs--like members of all families, similar but different.