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Krüppel-like factor KLF8 plays a critical role in adipocyte differentiation

Authors
 Haemi Lee  ;  Hyo Jung Kim  ;  Yoo Jeong Lee  ;  Min-Young Lee  ;  Hyeonjin Choi  ;  Hyemin Lee  ;  Jae-woo Kim 
Citation
 PLOS ONE, Vol.7(12) : e52474, 2012 
Journal Title
PLOS ONE
Issue Date
2012
MeSH
3T3-L1 Cells ; Adipocytes/cytology* ; Adipocytes/metabolism* ; Adipose Tissue/cytology ; Animals ; Base Sequence ; CCAAT-Enhancer-Binding Protein-alpha/genetics ; Cell Differentiation*/genetics ; Clone Cells ; Gene Expression Regulation ; Gene Knockdown Techniques ; Mice ; Mitosis ; Molecular Sequence Data ; PPAR gamma/genetics ; Promoter Regions, Genetic ; Protein Binding/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism* ; Transcription, Genetic
Keywords
3T3-L1 Cells ; Adipocytes/cytology* ; Adipocytes/metabolism* ; Adipose Tissue/cytology ; Animals ; Base Sequence ; CCAAT-Enhancer-Binding Protein-alpha/genetics ; Cell Differentiation*/genetics ; Clone Cells ; Gene Expression Regulation ; Gene Knockdown Techniques ; Mice ; Mitosis ; Molecular Sequence Data ; PPAR gamma/genetics ; Promoter Regions, Genetic ; Protein Binding/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism* ; Transcription, Genetic
Abstract
KLF8 (Krüppel-like factor 8) is a zinc-finger transcription factor known to play an essential role in the regulation of the cell cycle, apoptosis, and differentiation. However, its physiological roles and functions in adipogenesis remain unclear. In the present study, we show that KLF8 acts as a key regulator controlling adipocyte differentiation. In 3T3-L1 preadipocytes, we found that KLF8 expression was induced during differentiation, which was followed by expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα). Adipocyte differentiation was significantly attenuated by the addition of siRNA against KLF8, whereas overexpression of KLF8 resulted in enhanced differentiation. Furthermore, luciferase reporter assays demonstrated that overexpression of KLF8 induced PPARγ2 and C/EBPα promoter activity, suggesting that KLF8 is an upstream regulator of PPARγ and C/EBPα. The KLF8 binding sites were localized by site mutation analysis to -191 region in C/EBPα promoter and -303 region in PPARγ promoter, respectively. Taken together, these data reveal that KLF8 is a key component of the transcription factor network that controls terminal differentiation during adipogenesis.
Files in This Item:
T201204868.pdf Download
DOI
10.1371/journal.pone.0052474
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Jae Woo(김재우) ORCID logo https://orcid.org/0000-0001-5456-9495
Kim, Hyo Jung(김효정) ORCID logo https://orcid.org/0000-0002-3514-1247
Lee, Yoo Jeong(이유정)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/91733
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