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Article Dans Une Revue EMBO Reports Année : 2010

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

Résumé

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.

Dates et versions

hal-00457698 , version 1 (18-02-2010)

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Citer

Sang Jun Lee, Paul T Pfluger, Ji Young Kim, Ruben Nogueiras, Angeles Duran, et al.. A functional role for the p62-ERK1 axis in the control of energy homeostasis and adipogenesis.. EMBO Reports, 2010, epub ahead of print. ⟨10.1038/embor.2010.7⟩. ⟨hal-00457698⟩
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