| First Author | Yeh WC | Year | 1997 |
| Journal | Immunity | Volume | 7 |
| Issue | 5 | Pages | 715-25 |
| PubMed ID | 9390694 | Mgi Jnum | J:44360 |
| Mgi Id | MGI:1099940 | Doi | 10.1016/s1074-7613(00)80391-x |
| Citation | Yeh WC, et al. (1997) Early lethality, functional NF-kappaB activation, and increased sensitivity to TNF-induced cell death in TRAF2-deficient mice. Immunity 7(5):715-25 |
| abstractText | 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. |
