Title : Desipramine-induced apoptosis in human PC3 prostate cancer cells: activation of JNK kinase and caspase-3 pathways and a protective role of [Ca2+]i elevation.

Pub. Date : 2008 Aug 19

PMID : 18606486






5 Functional Relationships(s)
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1 Desipramine-induced apoptosis in human PC3 prostate cancer cells: activation of JNK kinase and caspase-3 pathways and a protective role of [Ca2+]i elevation. Desipramine mitogen-activated protein kinase 8 Homo sapiens
2 Immunoblotting data revealed that desipramine activated the phosphorylation of c-Jun NH2-terminal kinase (JNK), but not extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK). Desipramine mitogen-activated protein kinase 8 Homo sapiens
3 Immunoblotting data revealed that desipramine activated the phosphorylation of c-Jun NH2-terminal kinase (JNK), but not extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK). Desipramine mitogen-activated protein kinase 8 Homo sapiens
4 Immunoblotting data suggest that BAPTA/AM pretreatment enhanced desipramine-evoked JNK phosphorylation and caspase-3 cleavage. Desipramine mitogen-activated protein kinase 8 Homo sapiens
5 The results suggest that in PC3 cells, desipramine caused apoptosis via inducing JNK-associated caspase-3 activation, and [Ca2+]i rises may slow down or alleviate desipramine-induced cytotoxicity. Desipramine mitogen-activated protein kinase 8 Homo sapiens