Preparing your results

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

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.

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


  • Lee SJ
  • Pfluger PT
  • Kim JY
  • Nogueiras R
  • Duran A
  • Pagès G
  • Pouysségur J
  • Tschöp MH
  • Diaz-Meco MT
  • Moscat J


EMBO reports

Publication Data

March 2, 2010

Associated Grants

  • Agency: NIAID NIH HHS, Id: R01 AI072581
  • Agency: NCI NIH HHS, Id: R01 CA132847
  • Agency: NCI NIH HHS, Id: R01 CA134530
  • Agency: NIDDK NIH HHS, Id: R01 DK088107
  • Agency: NIAID NIH HHS, Id: R01-AI072581
  • Agency: NCI NIH HHS, Id: R01-CA132847
  • Agency: NCI NIH HHS, Id: R01-CA134530
  • Agency: NCI NIH HHS, Id: T32 CA117846

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