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首页> 外文期刊>Neuron >An Essential Role for a MEK-C/EBP Pathway during Growth Factor-Regulated Cortical Neurogenesis.
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An Essential Role for a MEK-C/EBP Pathway during Growth Factor-Regulated Cortical Neurogenesis.

机译：在生长因子调节的皮质神经发生过程中，MEK-C / EBP途径的重要作用。

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摘要

Mammalian neurogenesis is determined by an interplay between intrinsic genetic mechanisms and extrinsic cues such as growth factors. Here we have defined a signaling cascade, a MEK-C/EBP pathway, that is essential for cortical progenitor cells to become postmitotic neurons. Inhibition of MEK or of the C/EBP family of transcription factors inhibits neurogenesis while expression of a C/EBPbeta mutant that is a phosphorylation-mimic at a MEK-Rsk site enhances neurogenesis. C/EBP mediates this positive effect by direct transcriptional activation of neuron-specific genes such as Talpha1 alpha-tubulin. Conversely, inhibition of C/EBP-dependent transcription enhances CNTF-mediated generation of astrocytes from the same progenitor cells. Thus, activation of a MEK-C/EBP pathway enhances neurogenesis and inhibits gliogenesis, thereby providing a mechanism whereby growth factors can selectively bias progenitors to become neurons during development.
机译：哺乳动物的神经发生是由内在的遗传机制和外在线索（例如生长因子）之间的相互作用决定的。在这里，我们定义了一个信号级联，MEK-C / EBP途径，对于皮层祖细胞成为有丝分裂后神经元至关重要。抑制MEK或C / EBP转录因子家族可抑制神经发生，而在MEK-Rsk位点磷酸化的C / EBPbeta突变体的表达则可增强神经发生。 C / EBP通过神经元特异性基因（例如Talpha1α-微管蛋白）的直接转录激活来介导这种积极作用。相反，抑制C / EBP依赖性转录可增强CNTF介导的同一祖细胞星形胶质细胞的生成。因此，MEK-C / EBP途径的激活增强了神经发生并抑制了神经胶质发生，从而提供了一种机制，使生长因子可以选择性地使祖细胞在发育过程中变成神经元。

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