https://www.selleckchem.com/products/gw6471.html
TGF-β1, GAS5, HDAC4 were up-regulated, while miR-217 was down-regulated in bronchial mucosal tissues of asthmatic children and TGF-β1-treated BEAS-2B cells. TGF-β1 could reduce cell viability and induce apoptosis, while these effects could be reversed by downregulation of GAS5 or HDAC4. Mechanically, GAS5 acted as a sponge for miR-217 to regulate the expression of HDAC4. Furthermore, overexpression of HDAC4 rescued the effects of GAS5 knockdown on viability and apoptosis of TGF-β1-induced BEAS-2B cells. GAS5 knockdown induced cell viabil
Like
Comment
Share
