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10.1038/srep28648

http://scihub22266oqcxt.onion/10.1038/srep28648
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C4921850!4921850!27345868
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suck abstract from ncbi


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pmid27345868      Sci+Rep 2016 ; 6 (ä): ä
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  • Dexras1 links glucocorticoids to insulin-like growth factor-1 signaling in adipogenesis #MMPMID27345868
  • Kim HJ; Cha JY; Seok JW; Choi Y; Yoon BK; Choi H; Yu JH; Song SJ; Kim A; Lee H; Kim D; Han JY; Kim Jw
  • Sci Rep 2016[]; 6 (ä): ä PMID27345868show ga
  • Glucocorticoids are associated with obesity, but the underlying mechanism by which they function remains poorly understood. Previously, we showed that small G protein Dexras1 is expressed by glucocorticoids and leads to adipocyte differentiation. In this study, we explored the mechanism by which Dexras1 mediates adipogenesis and show a link to the insulin-like growth factor-1 (IGF-1) signaling pathway. Without Dexras1, the activation of MAPK and subsequent phosphorylation of CCAAT/enhancer binding protein ? (C/EBP?) is abolished, thereby inhibiting mitotic clonal expansion and further adipocyte differentiation. Dexras1 translocates to the plasma membrane upon insulin or IGF-1 treatment, for which the unique C-terminal domain (amino acids 223?276) is essential. Dexras1-dependent MAPK activation is selectively involved in the IGF-1 signaling, because another Ras protein, H-ras localized to the plasma membrane independently of insulin treatment. Moreover, neither epidermal growth factor nor other cell types shows Dexras1-dependent MAPK activation, indicating the importance of Dexras1 in IGF-1 signaling in adipogenesis. Dexras1 interacts with Shc and Raf, indicating that Dexras1-induced activation of MAPK is largely dependent on the Shc-Grb2-Raf complex. These results suggest that Dexras1 is a critical mediator of the IGF-1 signal to activate MAPK, linking glucocorticoid signaling to IGF-1 signaling in adipogenesis.
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