Muzio M, Natoli G, Saccani S, Levrero M, Mantovani A
Department of Immunology and Cell Biology, Mario Negri Institute, I-20157 Milan, Italy.
J Exp Med. 1998 Jun 15;187(12):2097-101. doi: 10.1084/jem.187.12.2097.
The human homologue of Drosophila Toll (hToll) is a recently cloned receptor of the interleukin 1 receptor (IL-1R) superfamily, and has been implicated in the activation of adaptive immunity. Signaling by hToll is shown to occur through sequential recruitment of the adapter molecule MyD88 and the IL-1R-associated kinase. Tumor necrosis factor receptor-activated factor 6 (TRAF6) and the nuclear factor kappaB (NF-kappaB)-inducing kinase (NIK) are both involved in subsequent steps of NF-kappaB activation. Conversely, a dominant negative version of TRAF6 failed to block hToll-induced activation of stress-activated protein kinase/c-Jun NH2-terminal kinases, thus suggesting an early divergence of the two pathways.
果蝇Toll蛋白的人类同源物（hToll）是白细胞介素1受体（IL-1R）超家族中最近克隆出的一种受体，并且与适应性免疫的激活有关。hToll信号传导是通过衔接分子MyD88和IL-1R相关激酶的顺序募集而发生的。肿瘤坏死因子受体激活因子6（TRAF6）和核因子κB（NF-κB）诱导激酶（NIK）都参与了NF-κB激活的后续步骤。相反，TRAF6的显性负性形式未能阻断hToll诱导的应激激活蛋白激酶/c-Jun氨基末端激酶的激活，因此表明这两条途径在早期就出现了分歧。
