Title | A functional role for the p62-ERK1 axis in the control of energy homeostasis and adipogenesis. |
Publication Type | Journal Article |
Year of Publication | 2010 |
Authors | Lee SJun, Pfluger PT, Kim JYoung, Nogueiras R, Duran A, Pagès G, Pouysségur J, Tschöp MH, Diaz-Meco MT, Moscat J |
Journal | EMBO Rep |
Volume | 11 |
Issue | 3 |
Pagination | 226-32 |
Date Published | 2010 Mar |
ISSN | 1469-3178 |
Keywords | Adipocytes, Adipogenesis, Animals, Cell Differentiation, Extracellular Signal-Regulated MAP Kinases, Fibroblasts, Humans, Insulin, Mice, Mice, Inbred C57BL, Mice, Knockout, Models, Genetic, Obesity, Recombinant Proteins, Transcription Factor TFIIH, Transcription Factors |
Abstract | In vivo genetic inactivation of the signalling adapter p62 leads to mature-onset obesity and insulin resistance, which correlate with reduced energy expenditure (EE) and increased adipogenesis, without alterations in feeding or locomotor functions. Enhanced extracellular signal-regulated kinase (ERK) activity in adipose tissue from p62-knockout (p62(-/-)) mice, and differentiating fibroblasts, suggested an important role for this kinase in the metabolic alterations of p62(-/-) mice. Here, we show that genetic inactivation of ERK1 in p62(-/-) mice reverses their increased adiposity and adipogenesis, lower EE and insulin resistance. These results establish genetically that p62 is a crucial regulator of ERK1 in metabolism. |
DOI | 10.1038/embor.2010.7 |
Alternate Journal | EMBO Rep |
PubMed ID | 20154642 |
Grant List | R01-CA134530 / CA / NCI NIH HHS / United States R01-AI072581 / AI / NIAID NIH HHS / United States R01-CA132847 / CA / NCI NIH HHS / United States |
Related Faculty:
Jorge Moscat, Ph.D. Maria Diaz-Meco Conde, Ph.D.