Citation Details
JNK-dependent release of mitochondrial protein, SMAC during apoptosis in multiple myeloma (MM) cells
| Authors | Chauhan D, Li G, Hideshima T, Podar K, Mitsiades C, Midsiades N, Munshi N, Kharbanda S, Anderson KC |
| In | J Biol Chem (2003) 278(20): 17593-17596 |
| Genes of Interest | JNK (c-Jun NH2-terminal kinase) |
| Cells used in publication | MM.1S Blood/Immune Cells Cell Lines Species: human Tissue Origin: blood |
| Substrate | Plasmid (general) |
| Application | Co-Transfection |
| Topics | Apoptosis Expression of dominant-negative protein Signal transduction |
| Research Area | Cancer Research/Cell Biology |
| Relevant Products | Cell Line Nucleofector Kit V |
Nucleofection Experiments
Smac (second mitochondria-derived activator of caspases) promotes apoptosis via activation of caspases. Also JNK (c-Jun NH2-terminal kinase) has been linked to apoptosis. However, the role of JNK in the release of mitochondrial Smac is unknown. To address this question the authors blocked JNK by nucleofecting MM.1S (multiple myeloma) cells with a dominant negative version of JNK (DN-JNK) or control vector. Transfected cells were treated with 2ME2 (to induce apoptosis) and analyzed for accumulation of Smac in the cytosol and cell viability. DN-JNF transfectants showed an abolished release of Smac to the cytosol and survived longer than cells transfected with the vector alone.
