Cdk4 promotes adipogenesis through PPARγ activation

Anna Abella, Pierre Dubus, Marcos Malumbres, Sushil G. Rane, Hiroaki Kiyokawa, Audrey Sicard, Françoise Vignon, Dominique Langin, Mariano Barbacid, Lluis Fajas*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

109 Scopus citations

Abstract

Cell cycle regulators such as E2F1 and retinoblastoma (RB) play crucial roles in the control of adipogenesis, mostly by controlling the transition between preadipocyte proliferation and adipocyte differentiation. The serine-threonine kinase cyclin-dependent kinase 4 (cdk4) works in a complex with D-type cyclins to phosphorylate RB, mediating the entry of cells into the cell cycle in response to external stimuli. Because cdk4 is an upstream regulator of the E2F-RB pathway, we tested whether cdk4 was a target for new factors that regulate adipogenesis. Here we find that cdk4 inhibition impairs adipocyte differentiation and function. Disruption of cdk4 or activating mutations in cdk4 in primary mouse embryonic fibroblasts results in reduced and increased adipogenic potential, respectively, of these cells. We show that the effects of cdk4 are not limited to the control of differentiation; cdk4 also participates in adipocyte function through activation of PPARγ.

Original languageEnglish (US)
Pages (from-to)239-249
Number of pages11
JournalCell Metabolism
Volume2
Issue number4
DOIs
StatePublished - Oct 2005

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology

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