https://www.selleckchem.com/products/sd-208.html
Knockdown of TTTY15 increased cell viability, and inhibited apoptosis of hypoxia-induced AC16 cells. TTTY15 bound to and inversely regulated let-7b. Likewise, MAPK6 was a target of let-7b and was negatively regulated by let-7b. Silencing of TTTY15 ameliorated the impact of let-7b downregulation or MAPK6 upregulation on hypoxia-induced cardiomyocyte injury. TTTY15 modulated MAPK6 enrichment by sponging let-7b. In conclusion, knockdown of TTTY15 suppressed hypoxia-induced cardiomyocyte injury through the let-7b/MAPK6 axis.Atrial fibrillati
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