Title : Dependency of 2-methoxyestradiol-induced mitochondrial apoptosis on mitotic spindle network impairment and prometaphase arrest in human Jurkat T cells.

Pub. Date : 2015 Apr 15

PMID : 25732194






3 Functional Relationships(s)
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1 Concomitant treatment of JT/Neo cells with 2-MeO-E2 and the G1/S blocking agent aphidicolin resulted in G1/S arrest and abrogation of all apoptotic events, including Cdk1 activation, phosphorylation of Bcl-2, Mcl-1 and Bim, and ROS accumulation. 2-Methoxyestradiol cyclin dependent kinase 1 Homo sapiens
2 The 2-MeO-E2-induced phosphorylation of Bcl-2 family proteins and mitochondrial apoptotic events were suppressed by a Cdk1 inhibitor, but not by an Aurora A kinase (AURKA), Aurora B kinase (AURKB), JNK, or p38 MAPK inhibitor. 2-Methoxyestradiol cyclin dependent kinase 1 Homo sapiens
3 These results demonstrate that the apoptogenic effect of 2-MeO-E2 (0.5-1.0 muM) was attributable to mitotic spindle defect-mediated prometaphase arrest, Cdk1 activation, phosphorylation of Bcl-2, Mcl-1, and Bim, and activation of Bak and mitochondria-dependent caspase cascade. 2-Methoxyestradiol cyclin dependent kinase 1 Homo sapiens