Pub. Date : 2008 Aug 19
PMID : 18606486
5 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
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 |