The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contains a death domain. It has been shown to play a central role in the physiological regulation of programmed cell death, and has been implicated in the pathogenesis of various malignancies and diseases of the immune system. The interaction of this receptor with its ligand allows the formation of a death-inducing signaling complex that includes Fas-associated death domain protein (FADD), caspase 8, and caspase 10. The autoproteolytic processing of the caspases in the complex triggers a downstream caspase cascade, and leads to apoptosis. This receptor has been also shown to activate NF-kappaB, MAPK3/ERK1, and MAPK8/JNK, and is found to be involved in transducing the proliferating signals in normal diploid fibroblast and T cells. Several alternatively spliced transcript variants have been described, some of which are candidates for nonsense-mediated mRNA decay (NMD). The isoforms lacking the transmembrane domain may negatively regulate the apoptosis mediated by the full length isoform. [provided by RefSeq, Mar 2011].
Latest Publications for our TNF Receptor Superfamily, Member 6 蛋白
Orlinick, Vaishnaw, Elkon, Chao: "Requirement of cysteine-rich repeats of the Fas receptor for binding by the Fas ligand." in: The Journal of biological chemistry, Vol. 272, Issue 46, pp. 28889-94, (1997) (PubMed).
Liles, Kiener, Ledbetter, Aruffo, Klebanoff: "Differential expression of Fas (CD95) and Fas ligand on normal human phagocytes: implications for the regulation of apoptosis in neutrophils." in: The Journal of experimental medicine, Vol. 184, Issue 2, pp. 429-40, (1996) (PubMed).
Tanaka, Suda, Takahashi, Nagata: "Expression of the functional soluble form of human fas ligand in activated lymphocytes." in: The EMBO journal, Vol. 14, Issue 6, pp. 1129-35, (1995) (PubMed).
Yang, Merćep, Ware, Ashwell: "Fas and activation-induced Fas ligand mediate apoptosis of T cell hybridomas: inhibition of Fas ligand expression by retinoic acid and glucocorticoids." in: The Journal of experimental medicine, Vol. 181, Issue 5, pp. 1673-82, (1995) (PubMed).
Cheng, Zhou, Liu, Shapiro, Brauer, Kiefer, Barr, Mountz: "Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule." in: Science (New York, N.Y.), Vol. 263, Issue 5154, pp. 1759-62, (1994) (PubMed).
Takahashi, Tanaka, Brannan, Jenkins, Copeland, Suda, Nagata: "Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand." in: Cell, Vol. 76, Issue 6, pp. 969-76, (1994) (PubMed).