Interferon signal transduction.

A Larner, N C Reich
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引用次数: 23

Abstract

The interferon signal transduction pathway initiates at a cell surface receptor and mediates the activation of target genes in the nucleus. The binding of interferon to a transmembrane receptor stimulates the activation of associated tyrosine kinases of the Janus kinase (JAK) family. Subsequently, latent cytoplasmic transcription factors are activated by tyrosine phosphorylation and function as signal transducers and activators of transcription (STATs). Advances in the field of interferon research have contributed to our understanding of signal transduction induced by many cytokines that also use JAK/STAT signaling pathways to activate early response genes. The specificity of signal activation by distinct cytokines that share these signaling components, and the molecular interaction of the signaling components with each other and their respective cytokine receptors represent major areas of research that are beginning to be elucidated. Signaling molecules other than the JAKs and STATs have also been found to be activated following interferon binding. In addition, the induction of type I interferon stimulated genes by double-stranded RNA in the absence of interferon provides another pathway of specific gene activation.

干扰素信号转导。
干扰素信号转导途径始于细胞表面受体,介导细胞核内靶基因的激活。干扰素与跨膜受体的结合刺激Janus激酶(JAK)家族相关酪氨酸激酶的激活。随后,潜伏的细胞质转录因子被酪氨酸磷酸化激活,并作为信号转导和转录激活因子(STATs)发挥作用。干扰素研究领域的进展有助于我们了解许多细胞因子诱导的信号转导,这些细胞因子也使用JAK/STAT信号通路激活早期反应基因。共享这些信号成分的不同细胞因子的信号激活的特异性,以及信号成分彼此之间及其各自的细胞因子受体的分子相互作用代表了正在开始阐明的主要研究领域。除了jak和STATs之外的信号分子也被发现在干扰素结合后被激活。此外,在缺乏干扰素的情况下,双链RNA诱导I型干扰素刺激基因为特异性基因激活提供了另一种途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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