https://www.selleckchem.com/products/gant61.html
Notably, TGF-β receptors were present in the midbody of both cell lines. In TGF-β1-treated fibroblasts, colchicine or Hedgehog pathway inhibitor 4 impaired the midbody formation, and attenuated the upregulation of canonical TGF-β/Smad signaling and α-SMA expression. These findings offer novel insight into the midbody as an active organelle involved in fibroblast-myofibroblast transition by mediating TGF-β/Smad signaling, which could be a potential therapeutic target.For single-atom (SA)-based catalysis, it is urgent to understand the nat
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