| First Author | Ventura JJ | Year | 2004 |
| Journal | Genes Dev | Volume | 18 |
| Issue | 23 | Pages | 2905-15 |
| PubMed ID | 15545623 | Mgi Jnum | J:94259 |
| Mgi Id | MGI:3511716 | Doi | 10.1101/gad.1223004 |
| Citation | Ventura JJ, et al. (2004) JNK potentiates TNF-stimulated necrosis by increasing the production of cytotoxic reactive oxygen species. Genes Dev 18(23):2905-15 |
| abstractText | The c-Jun NH(2)-terminal kinase (JNK) has been implicated in both cell death and survival responses to different stimuli. Here we reexamine the function of JNK in tumor necrosis factor (TNF)-stimulated cell death using fibroblasts isolated from wild-type, Mkk4(-/-) Mkk7(-/-), and Jnk1(-/-) Jnk2(-/-) mice. We demonstrate that JNK can act to suppress TNF-stimulated apoptosis. However, we find that JNK can also potentiate TNF-stimulated necrosis by increasing the production of reactive oxygen species (ROS). Together, these data indicate that JNK can shift the balance of TNF-stimulated cell death from apoptosis to necrosis. Increased necrosis may represent a contributing factor in stress-induced inflammatory responses mediated by JNK. |
