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The Smad3/Smad4/CDK9 complex promotes renal fibrosis in mice with unilateral ureteral obstruction.

Kidney international (2015-07-30)
Xinli Qu, Mengjie Jiang, Yu Bo Yang Sun, Xiaoyun Jiang, Ping Fu, Yi Ren, Die Wang, Lie Dai, Georgina Caruana, John F Bertram, David J Nikolic-Paterson, Jinhua Li
RÉSUMÉ

Transforming growth factor-β1 (TGF-β1)/Smad signaling has a central role in the pathogenesis of renal fibrosis. Smad3 and Smad4 are pro-fibrotic, while Smad2 is anti-fibrotic. However, these Smads form heterogeneous complexes, the functions of which are poorly understood. Here we studied Smad complex function in renal fibrosis using the mouse model of unilateral ureteric obstruction. Mice heterozygous for Smad3/4 (Smad3/4

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LDC000067 hydrochloride, ≥98% (HPLC)