Bonni A, Sun Y, Nadal-Vicens M, Bhatt A, Frank D A, Rozovsky I, Stahl N, Yancopoulos G D, Greenberg M E
Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
Science. 1997 Oct 17;278(5337):477-83. doi: 10.1126/science.278.5337.477.
A mechanism by which members of the ciliary neurotrophic factor (CNTF)-leukemia inhibitory factor cytokine family regulate gliogenesis in the developing mammalian central nervous system was characterized. Activation of the CNTF receptor promoted differentiation of cerebral cortical precursor cells into astrocytes and inhibited differentiation of cortical precursors along a neuronal lineage. Although CNTF stimulated both the Janus kinase-signal transducer and activator of transcription (JAK-STAT) and Ras-mitogen-activated protein kinase signaling pathways in cortical precursor cells, the JAK-STAT signaling pathway selectively enhanced differentiation of these precursors along a glial lineage. These findings suggest that cytokine activation of the JAK-STAT signaling pathway may be a mechanism by which cell fate is controlled during mammalian development.
一种睫状神经营养因子（CNTF）-白血病抑制因子细胞因子家族成员在发育中的哺乳动物中枢神经系统中调节神经胶质生成的机制得到了阐明。CNTF受体的激活促进大脑皮质前体细胞向星形胶质细胞分化，并抑制皮质前体细胞沿神经元谱系的分化。尽管CNTF在皮质前体细胞中刺激了Janus激酶-信号转导子和转录激活子（JAK-STAT）以及Ras-丝裂原活化蛋白激酶信号通路，但JAK-STAT信号通路选择性地增强了这些前体细胞沿神经胶质谱系的分化。这些发现表明，JAK-STAT信号通路的细胞因子激活可能是哺乳动物发育过程中细胞命运得以控制的一种机制。
