| First Author | Papadakis ES | Year | 2006 |
| Journal | FEBS Lett | Volume | 580 |
| Issue | 5 | Pages | 1320-6 |
| PubMed ID | 16458303 | Mgi Jnum | J:106899 |
| Mgi Id | MGI:3619752 | Doi | 10.1016/j.febslet.2006.01.053 |
| Citation | Papadakis ES, et al. (2006) The regulation of Bax by c-Jun N-terminal protein kinase (JNK) is a prerequisite to the mitochondrial-induced apoptotic pathway. FEBS Lett 580(5):1320-6 |
| abstractText | The signaling mechanism by which JNK affects mitochondria is critical to initiate apoptosis. Here we show that the absence of JNK provides a partial resistance to the toxic effect of the heavy metal cadmium. Both wild type and jnk-/- fibroblasts undergoing death exhibit cytosolic cytochrome c but, unlike wild type cells, the JNK-deficient fibroblasts do not display increased caspase activity and DNA fragmentation. The absence of apoptotic death correlates with a specific defect in activation of Bax. We conclude that JNK-dependent regulation of Bax is essential to mediate the apoptotic release of cytochrome c regardless of Bid and Bim activation. |
