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Biochemical and biophysical research communications, 2016-01, Vol.469 (3), p.552-558
2016
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Autor(en) / Beteiligte
Titel
c-Jun regulates adipocyte differentiation via the KLF15-mediated mode
Ist Teil von
  • Biochemical and biophysical research communications, 2016-01, Vol.469 (3), p.552-558
Ort / Verlag
United States: Elsevier Inc
Erscheinungsjahr
2016
Quelle
MEDLINE
Beschreibungen/Notizen
  • Abnormal adipocyte differentiation is implicated in the development of metabolic disorders such as obesity and type II diabetes. Thus, an in-depth understanding of the molecular mechanisms associated with adipocyte differentiation is the first step in overcoming obesity and its related metabolic diseases. Here, we examined the role of c-Jun as a transcription factor in adipocyte differentiation. c-Jun overexpression in murine 3T3-L1 preadipocytes significantly inhibited adipocyte differentiation. In addition, the expression level of KLF15, an upstream effector of the key adipogenic factors C/EBPα and PPARγ, was decreased upon the ectopic expression of c-Jun. We found that c-Jun inhibited basal and glucocorticoid receptor (GR)-induced promoter activities of KLF15. c-Jun directly bound near the glucocorticoid response element (GRE) sites in the KLF15 promoter and inhibited adjacent promoter occupancies of GR. Furthermore, the restoration of KLF15 expression in 3T3-L1 cells with the stable ectopic expression of c-Jun partially rescued adipocyte differentiation. Our results demonstrate that c-Jun can suppress adipocyte differentiation through the down-regulation of KLF15 at the transcriptional level. This study proposes a novel mechanism by which c-Jun regulates adipocyte differentiation. •c-Jun overexpression in 3T3-L1 preadipocytes inhibits adipocyte differentiation.•c-Jun inhibits glucocorticoid receptor (GR)-induced promoter activities of KLF15.•c-Jun binds near the glucocortidoid response elements (GREs) in the KLF15 promoter.•KLF15 expression partially rescues suppression of adipocyte differentiation by c-Jun.•c-Jun can suppress adipocyte differentiation through the down-regulation of KLF15.

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