First Author | Eby MT | Year | 2000 |
Journal | J Biol Chem | Volume | 275 |
Issue | 20 | Pages | 15336-42 |
PubMed ID | 10809768 | Mgi Jnum | J:62270 |
Mgi Id | MGI:1858661 | Doi | 10.1074/jbc.275.20.15336 |
Citation | Eby MT, et al. (2000) TAJ, a novel member of the tumor necrosis factor receptor family, activates the c-Jun N-terminal kinase pathway and mediates caspase-independent cell death. J Biol Chem 275(20):15336-42 |
abstractText | We have isolated a novel member of the TNFR family, designated TAJ, that is highly expressed during embryonic development. TAJ possesses a unique cytoplasmic domain with no sequence homology to the previously characterized members of the TNFR family. TAJ interacts with the TRAF family members and activates the JNK pathway when overexpressed in mammalian cells. Although it lacks a death domain, TAJ is capable of inducing apoptosis by a caspase-independent mechanism. Based on its unique expression profile and signaling properties, TAJ may play an essential role in embryonic development. |