Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

A functional role for the p62-ERK1 axis in the control of energy homeostasis and adipogenesis.

EMBO reports | Mar 2, 2010

http://www.ncbi.nlm.nih.gov/pubmed/20154642

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.

Pubmed ID: 20154642 RIS Download

Mesh terms: 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 Factors

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.