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PMID:16458303
| Citation |
Papadakis, ES, Finegan, KG, Wang, X, Robinson, AC, Guo, C, Kayahara, M and Tournier, C (2006) The regulation of Bax by c-Jun N-terminal protein kinase (JNK) is a prerequisite to the mitochondrial-induced apoptotic pathway. FEBS Lett. 580:1320-6 |
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| Abstract |
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. |
| Links |
PubMed Online version:10.1016/j.febslet.2006.01.053 |
| Keywords |
Animals; Apoptosis; Apoptosis Regulatory Proteins/metabolism; BH3 Interacting Domain Death Agonist Protein/metabolism; Cadmium/toxicity; Cells, Cultured; Cytochromes c/metabolism; Enzyme Activation; Fibroblasts/cytology; JNK Mitogen-Activated Protein Kinases/deficiency; JNK Mitogen-Activated Protein Kinases/metabolism; Membrane Proteins/metabolism; Mice; Mice, Knockout; Mitochondria/physiology; Proto-Oncogene Proteins/metabolism; Signal Transduction/physiology; bcl-2-Associated X Protein/metabolism |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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See also
References
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