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    Immunity. 1998 Mar;8(3):297-303.

    The death domain kinase RIP mediates the TNF-induced NF-kappaB signal.

    Kelliher MA, Grimm S, Ishida Y, Kuo F, Stanger BZ, Leder P.

    Source

    Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. kelliher@rascal.med.harvard.edu

    Abstract

    The death domain serine/threonine kinase RIP interacts with the death receptors Fas and tumor necrosis receptor 1 (TNFR1). In vitro, RIP stimulates apoptosis, SAPK/JNK, and NF-kappaB activation. To define the physiologic role(s) that RIP plays in regulating apoptosis in vivo, we introduced a rip null mutation in mice through homologous recombination. RIP-deficient mice appear normal at birth but fail to thrive, displaying extensive apoptosis in both the lymphoid and adipose tissue and dying at 1-3 days of age. In contrast to a normal thymic anti-Fas response, rip-/- cells are highly sensitive to TNFalpha-induced cell death. Sensitivity to TNFalpha-mediated cell death in rip-/- cells is accompanied by a failure to activate the transcription factor NF-kappaB.

    PMID:
    9529147
    [PubMed - indexed for MEDLINE]

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