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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

Authors

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

Journal

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