In Vitro |
Kongensin A (0-15 μM; 6 hours; HT29 cells) treatment induces caspase activation and apoptosis in multiple cancer cell lines in a dosage-dependent manner[1]. Kongensin A (0-15 μM; 24 hours; HT29 cells) treatment induces the degradation of RIPK1 and oncogenic kinases such as ERBB2, AKT, EGFR, and B-raf, and induces the up-regulation of HSP90A and HSP90B[1]. Kongensin A covalently binds to cysteine 420 in the middle domain of HSP90 and dissociates HSP90 from its cochaperone CDC37. The HSP90-CDC37 complex is required for RIP3 activation, KA blocks LPS/Smac mimetics/Z-VAD and RIP3 polymerization-induced cell death, in which cell death is dependent on RIP3 but not its upstream kinase RIP1[1]. Apoptosis Analysis[1] Cell Line: HT29 cells Concentration: 0 μM, 2.5 μM, 5 μM, 15 μM Incubation Time: 6 hours Result: Induced caspase activation and apoptosis in a dosage-dependent manner. Western Blot Analysis[1] Cell Line: HT29 cells Concentration: 0 μM, 2.5 μM, 5 μM, 15 μM Incubation Time: 24 hours Result: Induced the degradation of RIPK1 and oncogenic kinases such as ERBB2, AKT, EGFR, and B-raf, and induced the up-regulation of HSP90A and HSP90B.
|