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A functional role for the p62-ERK1 axis in the control of energy homeostasis and adipogenesis.
EMBO Rep. 11, 226-232 (2010)
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.
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Publication type
Article: Journal article
Document type
Scientific Article
Language
english
Publication Year
2010
HGF-reported in Year
0
ISSN (print) / ISBN
1469-221X
e-ISSN
1469-3178
Journal
EMBO Reports
Quellenangaben
Volume: 11,
Issue: 3,
Pages: 226-232
Publisher
EMBO Press
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)
PubMed ID
20154642
WOS ID
000275056700022
Erfassungsdatum
2010-12-31