Dissection of TNF receptor 1 effector functions: JNK activation is not linked to apoptosis while NF-kappaB activation prevents cell death.
摘要：
Through its type 1 receptor (TNFR1), the cytokine TNF elicits an unusually wide range of biological responses, including inflammation, tumor necrosis, cell proliferation, differentiation, and apoptosis. We investigated how TNFR1 activates different effector functions; the protein kinase JNK, transcription factor NF-kappaB, and apoptosis. We found that the three responses are mediated through separate pathways. Recruitment of the signal transducer FADD to the TNFR1 complex mediates apoptosis but not NF-kappaB or JNK activation. Two other signal transducers, RIP and TRAF2, mediate both JNK and NF-kappaB activation. These two responses, however, diverge downstream to TRAF2. Most importantly, JNK activation is not involved in induction of apoptosis, while activation of NF-kappaB protects against TNF-induced apoptosis.
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关键词：
Hela Cells Tumor Cells, Cultured Humans Adenocarcinoma Breast Neoplasms Fatty Acid Desaturases Protein Kinases Mitogen-Activated Protein Kinase Kinases MAP Kinase Kinase 4 JNK Mitogen-Activated Protein Kinases
DOI：
10.1016/S0092-8674(00)81375-6
被引量：
年份：
1996
Elsevier
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