Title : Imatinib induces H2AX phosphorylation and apoptosis in chronic myelogenous leukemia cells in vitro via caspase-3/Mst1 pathway.

Pub. Date : 2012 Apr

PMID : 22388075






5 Functional Relationships(s)
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1 Imatinib induces H2AX phosphorylation and apoptosis in chronic myelogenous leukemia cells in vitro via caspase-3/Mst1 pathway. Imatinib Mesylate caspase 3 Homo sapiens
2 Meanwhile, imatinib (1-8 mumol/L) activated caspase-3 and its downstream mammalian STE20-like kinase 1 (Mst1), and induced apoptosis of K562 cells. Imatinib Mesylate caspase 3 Homo sapiens
3 The caspase-3 inhibitor Z-VAD (40 mumol/L) reduced imatinib-induced H2AX phosphorylation at Ser139 and Tyr142 and blocked imatinib-induced apoptosis of K562 cells. Imatinib Mesylate caspase 3 Homo sapiens
4 The caspase-3 inhibitor Z-VAD (40 mumol/L) reduced imatinib-induced H2AX phosphorylation at Ser139 and Tyr142 and blocked imatinib-induced apoptosis of K562 cells. Imatinib Mesylate caspase 3 Homo sapiens
5 CONCLUSION: The caspase-3/Mst1 pathway is required for H2AX C-terminal phosphorylation at Ser139 and Tyr142 and subsequent apoptosis in Bcr-Abl-positive K562 cells induced by imatinib. Imatinib Mesylate caspase 3 Homo sapiens