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    JunD mediates survival signaling by the JNK signal transduction pathway

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    Authors
    Lamb, Jennifer A.
    Ventura, Juan-Jose
    Hess, Patricia M.
    Flavell, Richard A.
    Davis, Roger J.
    UMass Chan Affiliations
    Howard Hughes Medical Institute and Program in Molecular Medicine
    Graduate School of Biomedical Sciences
    Document Type
    Journal Article
    Publication Date
    2003-06-25
    Keywords
    Animals; Apoptosis; Cell Line; Cell Survival; DNA Fragmentation; Enzyme Activation; Fibroblasts; Gene Expression Regulation; Genes, Reporter; Mice; Mitogen-Activated Protein Kinases; Models, Biological; NF-kappa B; Protein Isoforms; Proto-Oncogene Proteins c-jun; *Signal Transduction; Time Factors; Transcription, Genetic; Tumor Necrosis Factor-alpha
    Life Sciences
    Medicine and Health Sciences
    
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    https://doi.org/10.1016/S1097-2765(03)00203-X
    Abstract
    The c-Jun NH(2)-terminal kinase (JNK) can cause cell death by activating the mitochondrial apoptosis pathway. However, JNK is also capable of signaling cell survival. The mechanism that accounts for the dual role of JNK in apoptosis and survival signaling has not been established. Here we demonstrate that JNK-stimulated survival signaling can be mediated by JunD. The JNK/JunD pathway can collaborate with NF-kappaB to increase antiapoptotic gene expression. This observation accounts for the ability of JNK to cause either survival or apoptosis in different cellular contexts. Furthermore, these data illustrate the general principal that signal transduction pathway integration is critical for the ability of cells to mount an appropriate biological response to a specific challenge.
    Source

    Mol Cell. 2003 Jun;11(6):1479-89.

    DOI
    10.1016/S1097-2765(03)00203-X
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/33986
    PubMed ID
    12820962
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    Link to article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1016/S1097-2765(03)00203-X
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