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Early lethality, functional NF-kappaB activation, and increased sensitivity to TNF-induced cell death in TRAF2-deficient mice.

Immunity | Nov 17, 1997

http://www.ncbi.nlm.nih.gov/pubmed/9390694

TRAF2 is an intracellular signal-transducing protein recruited to the TNFR1 and TNFR2 receptors following TNF stimulation. To investigate the physiological role of TRAF2, we generated TRAF2-deficient mice. traf2-/- mice appeared normal at birth but became progressively runted and died prematurely. Atrophy of the thymus and spleen and depletion of B cell precursors also were observed. Thymocytes and other hematopoietic progenitors were highly sensitive to TNF-induced cell death and serum TNF levels were elevated in these TRAF2-deficient animals. Examination of traf2-/- cells revealed a severe reduction in TNF-mediated JNK/SAPK activation but a mild effect on NF-kappaB activation. These results suggest that TRAF2-independent pathways of NF-kappaB activation exist and that TRAF2 is required for an NF-kappaB-independent signal that protects against TNF-induced apoptosis.

Pubmed ID: 9390694 RIS Download

Mesh terms: Animals | Calcium-Calmodulin-Dependent Protein Kinases | Cell Death | Cycloheximide | Enzyme Activation | Female | Hematopoietic Stem Cells | JNK Mitogen-Activated Protein Kinases | Liver | Male | Mice | Mice, Inbred C57BL | Mice, Knockout | Mitogen-Activated Protein Kinases | NF-kappa B | Protein Synthesis Inhibitors | Proteins | Receptors, Tumor Necrosis Factor | Signal Transduction | TNF Receptor-Associated Factor 2 | Tumor Necrosis Factor-alpha

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