| First Author | Kelliher MA | Year | 1998 |
| Journal | Immunity | Volume | 8 |
| Issue | 3 | Pages | 297-303 |
| PubMed ID | 9529147 | Mgi Jnum | J:46522 |
| Mgi Id | MGI:1201271 | Doi | 10.1016/s1074-7613(00)80535-x |
| Citation | Kelliher MA, et al. (1998) The death domain kinase RIP mediates the TNF-induced NF-kappaB signal. Immunity 8(3):297-303 |
| abstractText | The death domain serine/threonine kinase RIP interacts with the death receptors Fas and tumor necrosis receptor 1 (TNFR1). In vitro, RIP stimulates apoptosis, SAPK/JNK, and NF-kappaB activation. To define the physiologic role(s) that RIP plays in regulating apoptosis in vivo, we introduced a rip null mutation in mice through homologous recombination. RIP-deficient mice appear normal at birth but fail to thrive, displaying extensive apoptosis in both the lymphoid and adipose tissue and dying at 1-3 days of age. In contrast to a normal thymic anti-Fas response, rip-/- cells are highly sensitive to TNFalpha-induced cell death. Sensitivity to TNFalpha-mediated cell death in rip- /- cells is accompanied by a failure to activate the transcription factor NF-kappaB. |
