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Oct4 或 Nanog 敲低诱导的小鼠胚胎干细胞生长停滞和细胞凋亡:Trp53 的可能作用。

Cell growth arrest and apoptosis induced by Oct4 or Nanog knockdown in mouse embryonic stem cells: a possible role of Trp53.

机构信息

Institute of Reproduction and Stem Cell Engineering, Central South University, 110 Xiangya Road, Changsha, 410078 Hunan, China.

出版信息

Mol Biol Rep. 2012 Feb;39(2):1855-61. doi: 10.1007/s11033-011-0928-6. Epub 2011 Jun 26.

Abstract

It has been clear that both Oct4 and Nanog play essential roles in maintaining embryonic stem cells (ESCs) undifferentiation. However, the roles of Oct4 and Nanog in ESCs growth and apoptosis have been much less explored. In this study, we systematically examined the effects of Oct4 or Nanog knockdown on mouse ESCs (mESCs) growth and apoptosis as well as potential mechanisms. Our results show that Oct4 or Nanog knockdown induces growth arrest and apoptosis in mESCs, indicating that the two genes also play important roles in mESCs survival and growth. Moreover, upregulation in Trp53 and its downstream genes expression was detected in Oct4 or Nanog knockdown mESCs, suggesting a possible role of Trp53 in Oct4 or Nanog knockdown induced mESCs growth arrest and apoptosis.

摘要

很明显,Oct4 和 Nanog 在维持胚胎干细胞(ESCs)未分化状态方面都发挥着重要作用。然而,Oct4 和 Nanog 在 ESCs 生长和凋亡中的作用却鲜有人探索。在这项研究中,我们系统地研究了敲低 Oct4 或 Nanog 对小鼠胚胎干细胞(mESCs)生长和凋亡的影响及其潜在机制。结果表明,敲低 Oct4 或 Nanog 会诱导 mESCs 生长停滞和凋亡,这表明这两个基因在 mESCs 的存活和生长中也起着重要作用。此外,在敲低 Oct4 或 Nanog 的 mESCs 中检测到 Trp53 及其下游基因表达上调,表明 Trp53 可能在 Oct4 或 Nanog 敲低诱导的 mESCs 生长停滞和凋亡中发挥作用。

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