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"A functional role for the p62-ERK1 axis in the control of energy homeostasis and adipogenesis." |
Lee SJ, Pfluger PT, Kim JY, Nogueiras R, Duran A, Pages G, Pouyssegur J, Tschop MH, Diaz-Meco MT, Moscat J |
Published March 1, 2010 in EMBO Rep volume 11 .
Pubmed ID: 20154642
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. |
This publication refers to following REPAIRtoire entries:
| Genes |
Last modification of this entry: Oct. 6, 2010
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