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Bisindoylmaleimide I suppresses adipocyte differentiation through stabilization of intracellular {beta}-catenin protein

Journal Article · · Biochemical and Biophysical Research Communications
; ;  [1];  [2];  [3];  [1];  [1]
  1. PharmacoGenomics Research Center, Inje University, Busan 614-735 (Korea, Republic of)
  2. Department of Bioscience and Biotechnology, Konkuk University, Seoul 143-701 (Korea, Republic of)
  3. Department of Biochemistry, College of Medicine, Inje University, Busan 614-735 (Korea, Republic of)
The Wnt/{beta}-catenin signaling pathway plays important roles in cell differentiation. Activation of this pathway, likely by Wnt-10b, has been shown to inhibit adipogenesis in cultured 3T3-L1 preadipocytes and mice. Here we revealed that bisindoylmaleimide I (BIM), which is widely used as a specific inhibitor of protein kinase C (PKC), inhibits adipocyte differentiation through activation of the Wnt/{beta}-catenin signaling pathway. BIM increased {beta}-catenin responsive transcription (CRT) and up-regulated intracellular {beta}-catenin levels in HEK293 cells and 3T3-L1 preadipocytes. BIM significantly decreased intracellular lipid accumulation and reduced expression of important adipocyte marker genes including peroxisome-proliferator-activated receptor {gamma} (PPAR{gamma}) and CAATT enhancer-binding protein {alpha} (C/EBP{alpha}) in 3T3-L1 preadipocytes. Taken together, our findings indicate that BIM inhibits adipogenesis by increasing the stability of {beta}-catenin protein in 3T3-L1 preadipocyte cells.
OSTI ID:
21043640
Journal Information:
Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 1 Vol. 367; ISSN 0006-291X; ISSN BBRCA9
Country of Publication:
United States
Language:
English

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