肿瘤坏死因子超家族激活的信号转导衔接蛋白和信号通路。
The signaling adaptors and pathways activated by TNF superfamily.
作者信息
Dempsey Paul W, Doyle Sean E, He Jeannie Q, Cheng Genhong
机构信息
Department of Microbiology, Jonsson Comprehensive Cancer Center, University of California at Los Angeles, 8-240 Factor Building, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA.
出版信息
Cytokine Growth Factor Rev. 2003 Jun-Aug;14(3-4):193-209. doi: 10.1016/s1359-6101(03)00021-2.
Members of the TNF receptor superfamily play pivotal roles in numerous biological events in metazoan organisms. Ligand-mediated trimerization by corresponding homo- or heterotrimeric ligands, the TNF family ligands, causes recruitment of several intracellular adaptors, which activate multiple signal transduction pathways. While recruitment of death domain (DD) containing adaptors such as Fas associated death domain (FADD) and TNFR associated DD (TRADD) can lead to the activation of a signal transduction pathway that induces apoptosis, recruitment of TRAF family proteins can lead to the activation of transcription factors such as, NF-kappaB and JNK thereby promoting cell survival and differentiation as well as immune and inflammatory responses. Individual TNF receptors are expressed in different cell types and have a range of affinities for various intracellular adaptors, which provide tremendous signaling and biological specificities. In addition, numerous signaling modulators are involved in regulating activities of signal transduction pathways downstream of receptors in this superfamily. Most of the TNF receptor superfamily members as well as many of their signaling mediators, have been uncovered in the last two decades. However, much remains unknown about how individual signal transduction pathways are regulated upon activation by any particular TNF receptor, under physiological conditions.
肿瘤坏死因子受体超家族成员在多细胞生物的众多生物学事件中发挥着关键作用。配体介导的三聚化作用由相应的同三聚体或异三聚体配体(肿瘤坏死因子家族配体)引发,这会导致几种细胞内衔接蛋白的募集,进而激活多条信号转导通路。当募集含有死亡结构域(DD)的衔接蛋白,如Fas相关死亡结构域(FADD)和肿瘤坏死因子受体相关死亡结构域(TRADD)时,可导致诱导细胞凋亡的信号转导通路的激活;而募集肿瘤坏死因子受体相关因子(TRAF)家族蛋白则可导致转录因子如核因子κB(NF-κB)和应激活化蛋白激酶(JNK)的激活,从而促进细胞存活与分化以及免疫和炎症反应。单个肿瘤坏死因子受体在不同细胞类型中表达,并且对各种细胞内衔接蛋白具有一系列亲和力,这提供了巨大的信号传导和生物学特异性。此外,众多信号调节因子参与调节该超家族受体下游信号转导通路的活性。在过去二十年中,大多数肿瘤坏死因子受体超家族成员及其许多信号传导介质已被发现。然而,在生理条件下,任何特定肿瘤坏死因子受体激活后,单个信号转导通路如何被调节,仍有许多未知之处。