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10.1155/2014/782625

http://scihub22266oqcxt.onion/10.1155/2014/782625
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C4058256!4058256!24971350
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suck abstract from ncbi


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pmid24971350      Biomed+Res+Int 2014 ; 2014 (ä): ä
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  • High Glucose Induces Sumoylation of Smad4 via SUMO2/3 in Mesangial Cells #MMPMID24971350
  • Zhou X; Gao C; Huang W; Yang M; Chen G; Jiang L; Gou F; Feng H; Ai N; Xu Y
  • Biomed Res Int 2014[]; 2014 (ä): ä PMID24971350show ga
  • Recent studies have shown that sumoylation is a posttranslational modification involved in regulation of the transforming growth factor-? (TGF-?) signaling pathway, which plays a critical role in renal fibrosis in diabetic nephropathy (DN). However, the role of sumoylation in the regulation of TGF-? signaling in DN is still unclear. In the present study, we investigated the expression of SUMO (SUMO1 and SUMO2/3) and Smad4 and the interaction between SUMO and Smad4 in cultured rat mesangial cells induced by high glucose. We found that SUMO1 and SUMO2/3 expression was significantly increased in the high glucose groups compared to the normal group (P < 0.05). Smad4 and fibronectin (FN) levels were also increased in the high glucose groups in a dose-dependent manner. Coimmunoprecipitation and confocal laser scanning revealed that Smad4 interacted and colocalized with SUMO2/3, but not with SUMO1 in mesangial cells. Sumoylation (SUMO2/3) of Smad4 under high glucose condition was strongly enhanced compared to normal control (P < 0.05). These results suggest that high glucose may activate TGF-?/Smad signaling through sumoylation of Samd4 by SUMO2/3 in mesangial cells.
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