Ma Xinwei, Chen Haixia, Chen Lingyi
State Key Laboratory of Medicinal Chemical Biology, Collaborative Innovation Center for Biotherapy, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Protein Sciences and College of Life Sciences, Nankai University, Tianjin, China.
State Key Laboratory of Medicinal Chemical Biology, Collaborative Innovation Center for Biotherapy, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Protein Sciences and College of Life Sciences, Nankai University, Tianjin, China.
Exp Hematol. 2016 Mar;44(3):151-6. doi: 10.1016/j.exphem.2015.12.008. Epub 2016 Jan 2.
Erk signaling plays a critical role in maintaining the pluripotency of mouse embryonic stem cells (ESCs). Inhibition of Mek/Erk signaling by pharmacologic Mek inhibitor promotes self-renewal and pluripotency of mouse ESCs. However, knockout of Erk1/2 genes compromises the self-renewal and genomic stability of mouse ESCs. In this review, we summarize recent progress in understanding the role of Erk signaling in pluripotency maintenance, discuss the dual role of Erk in mouse ESCs, and provide explanations for the conflicting data regarding Mek inhibition and Erk knockout. Remaining questions and the prospects of Erk signaling in pluripotency maintenance are also discussed.
细胞外调节蛋白激酶(Erk)信号传导在维持小鼠胚胎干细胞(ESC)的多能性方面起着关键作用。用药物性Mek抑制剂抑制Mek/Erk信号传导可促进小鼠胚胎干细胞的自我更新和多能性。然而,敲除Erk1/2基因会损害小鼠胚胎干细胞的自我更新和基因组稳定性。在这篇综述中,我们总结了在理解Erk信号传导在多能性维持中的作用方面的最新进展,讨论了Erk在小鼠胚胎干细胞中的双重作用,并对有关Mek抑制和Erk敲除的相互矛盾的数据提供了解释。还讨论了关于Erk信号传导在多能性维持方面的遗留问题和前景。