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

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


  • Yeh WC
  • Shahinian A
  • Speiser D
  • Kraunus J
  • Billia F
  • Wakeham A
  • de la Pompa JL
  • Ferrick D
  • Hum B
  • Iscove N
  • Ohashi P
  • Rothe M
  • Goeddel DV
  • Mak TW



Publication Data

November 17, 1997

Associated Grants


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