| First Author | Lee SJ | Year | 2010 |
| Journal | EMBO Rep | Volume | 11 |
| Issue | 3 | Pages | 226-32 |
| PubMed ID | 20154642 | Mgi Jnum | J:160384 |
| Mgi Id | MGI:4454368 | Doi | 10.1038/embor.2010.7 |
| Citation | Lee SJ, et al. (2010) A functional role for the p62-ERK1 axis in the control of energy homeostasis and adipogenesis. EMBO Rep 11(3):226-32 |
| abstractText | 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. |
