Dephosphorylation of CCAAT/enhancer-binding protein β by protein phosphatase 2A containing B56δ is required at the early time of adipogenesis

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Title
Dephosphorylation of CCAAT/enhancer-binding protein β by protein phosphatase 2A containing B56δ is required at the early time of adipogenesis
Author(s)
M Park; Y A Choi; Hee Gu Lee; K I Kim; J S Lim; M S Lee; K S Oh; Y Yang
Bibliographic Citation
Biochimica et Biophysica Acta-Molecular and Cell Biology of Lipids, vol. 1841, no. 11, pp. 1608-1618
Publication Year
2014
Abstract
It is known that protein phosphatase 2A (PP2A) expression is increased in high-fat diet (HFD)-induced obese mice, but the role of PP2A in adipogenesis as well as obesity remains to be addressed. In this study, the role of PP2A in adipogenesis was explored. Preadipocytes were treated with okadaic acid (OA) during adipogenesis and the degree of adipogenesis was determined. The OA treatment blocked adipogenesis at the early time of adipogenesis, but not at the late time. In the early time of adipogenesis, CCAAT/enhancer-binding protein β (C/EBPβ) activation is preceded by the expression of key adipogenic transcription factors including PPARγ and C/EBPα, which function at the late time of adipogenesis, and then C/EBPβ is degraded. However, the inhibition of PP2A by OA treatment sustained phosphorylation of C/EBPβ and delayed its degradation. In turn, PPARγ and C/EBPα activation was altered. Among the various regulatory B56 subunits consisting of PP2A holoenzyme, B56δ was directly bound to C/EBPβ and was responsible for the dephosphorylation of C/EBPβ by PP2A. Taken together, these findings suggest that the phosphorylation of C/EBPβ after hormonal induction has to be inactivated by PP2A containing B56δ at the early time of adipogenesis to allow the completion of adipogenesis.
Keyword
AdipogenesisB56δC/EBPβExtracellular signal regulated kinase (ERK)Protein phosphatase 2A (PP2A)
ISSN
1388-1981
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.bbalip.2014.08.008
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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