• 中文核心期刊要目总览
  • 中国科技核心期刊
  • 中国科学引文数据库(CSCD)
  • 中国科技论文与引文数据库(CSTPCD)
  • 中国学术期刊文摘数据库(CSAD)
  • 中国学术期刊(网络版)(CNKI)
  • 中文科技期刊数据库
  • 万方数据知识服务平台
  • 中国超星期刊域出版平台
  • 国家科技学术期刊开放平台
  • 荷兰文摘与引文数据库(SCOPUS)
  • 日本科学技术振兴机构数据库(JST)
杨昕淳, 吴晓龙, 李文豪, 吴筱洁, 沈巧艳, 李云香, 彭莎, 华进联. 2022: OCT6通过调节MAPK和PI3K信号通路抑制猪诱导的多能干细胞分化. 动物学研究, 43(6): 911-922. DOI: 10.24272/j.issn.2095-8137.2022.220
引用本文: 杨昕淳, 吴晓龙, 李文豪, 吴筱洁, 沈巧艳, 李云香, 彭莎, 华进联. 2022: OCT6通过调节MAPK和PI3K信号通路抑制猪诱导的多能干细胞分化. 动物学研究, 43(6): 911-922. DOI: 10.24272/j.issn.2095-8137.2022.220
Xin-Chun Yang, Xiao-Long Wu, Wen-Hao Li, Xiao-Jie Wu, Qiao-Yan Shen, Yun-Xiang Li, Sha Peng, Jin-Lian Hua. 2022: OCT6 inhibits differentiation of porcine-induced pluripotent stem cells through MAPK and PI3K signaling regulation. Zoological Research, 43(6): 911-922. DOI: 10.24272/j.issn.2095-8137.2022.220
Citation: Xin-Chun Yang, Xiao-Long Wu, Wen-Hao Li, Xiao-Jie Wu, Qiao-Yan Shen, Yun-Xiang Li, Sha Peng, Jin-Lian Hua. 2022: OCT6 inhibits differentiation of porcine-induced pluripotent stem cells through MAPK and PI3K signaling regulation. Zoological Research, 43(6): 911-922. DOI: 10.24272/j.issn.2095-8137.2022.220

OCT6通过调节MAPK和PI3K信号通路抑制猪诱导的多能干细胞分化

OCT6 inhibits differentiation of porcine-induced pluripotent stem cells through MAPK and PI3K signaling regulation

  • 摘要: 作为POU家族的转录因子,OCT6在干细胞发育和分化中发挥着不同的作用,但其在猪诱导多能干细胞(PiPSCs)中的作用尚不清楚。在此,我们探讨了OCT6在PiPSCs中的作用。我们发现过表达OCT6的piPSCs在分化条件下能够保持克隆形态和多能性,其基因表达模式与未分化的piPSCs相似。功能分析表明,OCT6通过激活PI3K-AKT信号通路,减轻了抑制ERK信号通路对piPSC多能性的不利影响。我们的研究为OCT6促进多能干细胞维持的机制提供了新的线索。

     

    Abstract: As a transcription factor of the Pit-Oct-Unc (POU) domain family, octamer-binding transcription factor 6 (OCT6) participates in various aspects of stem cell development and differentiation. At present, however, its role in porcine-induced pluripotent stem cells (piPSCs) remains unclear. Here, we explored the function of OCT6 in piPSCs. We found that piPSCs overexpressing OCT6 maintained colony morphology and pluripotency under differentiation conditions, with a similar gene expression pattern to that of non-differentiated piPSCs. Functional analysis revealed that OCT6 attenuated the adverse effects of extracellular signal-regulated kinase (ERK) signaling pathway inhibition on piPSC pluripotency by activating phosphatidylinositol 3-kinase-protein kinase B (PI3K-AKT) signaling activity. Our research sheds new light on the mechanism by which OCT6 promotes PSC maintenance.

     

/

返回文章
返回