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Krüppel-like transcription factor KLF5 is a key regulator of adipocyte differentiation.

Authors
  • Oishi, Yumiko
  • Manabe, Ichiro
  • Tobe, Kazuyuki
  • Tsushima, Kensuke
  • Shindo, Takayuki
  • Fujiu, Katsuhito
  • Nishimura, Go
  • Maemura, Koji
  • Yamauchi, Toshimasa
  • Kubota, Naoto
  • Suzuki, Ryo
  • Kitamura, Toshio
  • Akira, Shizuo
  • Kadowaki, Takashi
  • Nagai, Ryozo
Type
Published Article
Journal
Cell Metabolism
Publisher
Elsevier
Publication Date
Jan 01, 2005
Volume
1
Issue
1
Pages
27–39
Identifiers
PMID: 16054042
Source
Medline
License
Unknown

Abstract

Krüppel-like factor 5 (KLF5) is a zinc-finger transcription factor known to play a pivotal role in the pathogenesis of cardiovascular disease. Here, we show that neonatal heterozygous KLF5 knockout mice exhibit a marked deficiency in white adipose tissue development, suggesting that KLF5 is also required for adipogenesis. In 3T3-L1 preadipocytes, KLF5 expression was induced at an early stage of differentiation, and this was followed by expression of PPARgamma2. Constitutive overexpression of dominant-negative KLF5 inhibited adipocyte differentiation, whereas overexpression of wild-type KLF5 induced differentiation even without hormonal stimulation. Moreover, embryonic fibroblasts obtained from KLF5+/- mice showed much attenuated adipocyte differentiation, confirming the key role played by KLF5 in adipocyte differentiation. KLF5 expression is induced by C/EBPbeta and delta. KLF5, in turn, acts in concert with C/EBPbeta/delta to activate the PPARgamma2 promoter. This study establishes KLF5 as a key component of the transcription factor network controlling adipocyte differentiation.

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