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    Genes Dev. 2004 Dec 1;18(23):2905-15. Epub 2004 Nov 15.

    JNK potentiates TNF-stimulated necrosis by increasing the production of cytotoxic reactive oxygen species.

    Ventura JJ, Cogswell P, Flavell RA, Baldwin AS Jr, Davis RJ.

    Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.

    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.

    PMID: 15545623 [PubMed - indexed for MEDLINE]

    PMCID: PMC534651

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