• Register
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.


Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.


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