Stahl N, Farruggella T J, Boulton T G, Zhong Z, Darnell J E, Yancopoulos G D
Regeneron Pharmaceuticals, Inc., Tarrytown, NY 10591.
Science. 1995 Mar 3;267(5202):1349-53. doi: 10.1126/science.7871433.
Many members of the cytokine receptor superfamily initiate intracellular signaling by activating members of the Jak family of tyrosine kinases. Activation of the same Jaks by multiple cytokines raises the question of how these cytokines activate distinct intracellular signaling pathways. Selection of particular substrates--the transcriptional activator Stat3 and protein tyrosine phosphatase PTP1D--that characterize responses to the ciliary neurotrophic factor-interleukin-6 cytokine family depended not on which Jak was activated, but was instead determined by specific tyrosine-based motifs in the receptor components--gp130 and LIFR--shared by these cytokines. Further, these tyrosine-based motifs were modular, because addition of a Stat3-specifying motif to another cytokine receptor, that for erythropoietin, caused it to activate Stat3 in a ligand-dependent fashion.
细胞因子受体超家族的许多成员通过激活酪氨酸激酶Jak家族的成员来启动细胞内信号传导。多种细胞因子对同一Jaks的激活引发了一个问题,即这些细胞因子如何激活不同的细胞内信号通路。对睫状神经营养因子-白细胞介素-6细胞因子家族反应具有特征性的特定底物——转录激活因子Stat3和蛋白酪氨酸磷酸酶PTP1D的选择,并不取决于激活的是哪种Jak,而是由这些细胞因子共有的受体成分——gp130和LIFR中特定的基于酪氨酸的基序决定的。此外,这些基于酪氨酸的基序是模块化的,因为将一个Stat3特异性基序添加到另一种细胞因子受体(即促红细胞生成素受体)上,会使其以配体依赖的方式激活Stat3。