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Updated: Mar 28, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
c-Jun regulates adipocyte differentiation via the KLF15-mediated mode
Da Som Lee1, Hyeonjin Choi1, Baek Soo Han2
1Functional Genomics Research Center, KRIBB, Daejeon 305-806, Republic of Korea.
Transcription factor c-Jun suppresses adipocyte differentiation by down-regulating KLF15. This discovery offers new insights into molecular mechanisms underlying obesity and type II diabetes.
Area of Science:
- Molecular Biology
- Cell Biology
- Metabolic Research
Background:
- Abnormal adipocyte differentiation contributes to metabolic disorders like obesity and type II diabetes.
- Understanding adipocyte differentiation mechanisms is crucial for addressing these diseases.
Purpose of the Study:
- To investigate the role of the transcription factor c-Jun in adipocyte differentiation.
- To elucidate the molecular mechanisms by which c-Jun influences adipogenesis.
Main Methods:
- Overexpression of c-Jun in murine 3T3-L1 preadipocytes.
- Analysis of KLF15 expression and promoter activity.
- Chromatin immunoprecipitation to assess protein-DNA binding.
- Restoration of KLF15 expression to evaluate rescue effects.
Main Results:
- Ectopic expression of c-Jun significantly inhibited adipocyte differentiation.
- c-Jun overexpression decreased KLF15 expression and repressed its promoter activity, including glucocorticoid receptor (GR)-induced activity.
- c-Jun directly bound near the KLF15 promoter's glucocorticoid response element (GRE) sites, inhibiting GR binding.
- Restoring KLF15 partially rescued adipocyte differentiation in c-Jun overexpressing cells.
Conclusions:
- c-Jun suppresses adipocyte differentiation by transcriptionally down-regulating KLF15.
- This study reveals a novel mechanism for c-Jun in regulating adipocyte differentiation.
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