Bertin J, Nir W J, Fischer C M, Tayber O V, Errada P R, Grant J R, Keilty J J, Gosselin M L, Robison K E, Wong G H, Glucksmann M A, DiStefano P S
Millennium Pharmaceuticals, Inc., Cambridge, Massachusetts 02139, USA.
J Biol Chem. 1999 May 7;274(19):12955-8. doi: 10.1074/jbc.274.19.12955.
The nematode CED-4 protein and its human homolog Apaf-1 play a central role in apoptosis by functioning as direct activators of death-inducing caspases. A novel human CED-4/Apaf-1 family member called CARD4 was identified that has a domain structure strikingly similar to the cytoplasmic, receptor-like proteins that mediate disease resistance in plants. CARD4 interacted with the serine-threonine kinase RICK and potently induced NF-kappaB activity through TRAF-6 and NIK signaling molecules. In addition, coexpression of CARD4 augmented caspase-9-induced apoptosis. Thus, CARD4 coordinates downstream NF-kappaB and apoptotic signaling pathways and may be a component of the host innate immune response.
线虫CED - 4蛋白及其人类同源物Apaf - 1作为死亡诱导半胱天冬酶的直接激活剂，在细胞凋亡中起核心作用。一种名为CARD4的新型人类CED - 4/Apaf - 1家族成员被鉴定出来，其结构域结构与介导植物抗病性的细胞质受体样蛋白惊人地相似。CARD4与丝氨酸 - 苏氨酸激酶RICK相互作用，并通过TRAF - 6和NIK信号分子有效诱导NF - κB活性。此外，CARD4的共表达增强了caspase - 9诱导的细胞凋亡。因此，CARD4协调下游NF - κB和凋亡信号通路，可能是宿主先天免疫反应的一个组成部分。
