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    JNK phosphorylation of Bim-related members of the Bcl2 family induces Bax-dependent apoptosis

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    Authors
    Lei, Kui
    Davis, Roger J.
    UMass Chan Affiliations
    Howard Hughes Medical Institute and Program in Molecular Medicine
    Document Type
    Journal Article
    Publication Date
    2003-02-20
    Keywords
    *Adaptor Proteins, Signal Transducing
    *Apoptosis
    Apoptosis Regulatory Proteins
    Carrier Proteins
    Cell Line
    DNA Mutational Analysis
    DNA, Complementary
    Fibroblasts
    Humans
    *Membrane Proteins
    Mitochondria
    Models, Biological
    Neurons
    Phosphorylation
    Plasmids
    Protein Binding
    Protein Isoforms
    Proto-Oncogene Proteins
    Proto-Oncogene Proteins c-bcl-2
    Signal Transduction
    Threonine
    bcl-2-Associated X Protein
    Life Sciences
    Medicine and Health Sciences
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC151358/
    Abstract
    The c-Jun NH(2)-terminal kinase (JNK) is activated when cells are exposed to environmental stress, including UV radiation. Gene disruption studies demonstrate that JNK is essential for UV-stimulated apoptosis mediated by the mitochondrial pathway by a Bax/Bak-dependent mechanism. Here, we demonstrate that JNK phosphorylates two members of the BH3-only subgroup of Bcl2-related proteins (Bim and Bmf) that are normally sequestered by binding to dynein and myosin V motor complexes. Phosphorylation by JNK causes release from the motor complexes. These proapoptotic BH3-only proteins therefore provide a molecular link between the JNK signal transduction pathway and the Bax/Bak-dependent mitochondrial apoptotic machinery.
    Source

    Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2432-7. Epub 2003 Feb 18. Link to article on publisher's site

    DOI
    10.1073/pnas.0438011100
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/38943
    PubMed ID
    12591950
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    Link to Article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1073/pnas.0438011100
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      Role of the Raf/mitogen-activated protein kinase pathway in p21ras desensitization

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