Baker S J, Reddy E P
Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Oncogene. 1996 Jan 4;12(1):1-9.
Signal transduction pathways which are initiated by members of the TNF superfamily utilize receptors which are devoid of intrinsic catalytic activity. Isolation and characterization of death domain (TNF-RI, Fas, TRADD, FADD/MORT-1, RIP) and TRAF domain-containing proteins (TRAF-1, TRAF-2, TRAF-3) have partially bridged a large molecular gap within one of several signaling pathways which originate at the plasma membrane and terminate in the nucleus. The ability of these two protein families to selectively dimerize and bind to related receptors allows them to govern diverse cellular responses which culminate in cellular proliferation, differentiation, effector functions, and apoptosis.
由肿瘤坏死因子(TNF)超家族成员启动的信号转导途径利用缺乏内在催化活性的受体。死亡结构域(TNF-RI、Fas、TRADD、FADD/MORT-1、RIP)和含TRAF结构域的蛋白质(TRAF-1、TRAF-2、TRAF-3)的分离和表征部分填补了起源于质膜并终止于细胞核的几种信号通路之一中的一个大分子间隙。这两个蛋白质家族选择性二聚化并与相关受体结合的能力使它们能够控制多种细胞反应,最终导致细胞增殖、分化、效应功能和凋亡。