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PHLDA3 通过激活 Akt-GSK3β 通路来阻碍体细胞核重编程。

PHLDA3 impedes somatic cell reprogramming by activating Akt-GSK3β pathway.

机构信息

CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Cell and Molecular Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science & Technology of China, Hefei, 230027, China.

Department of Immunology, Anhui Medical University, Hefei, 230032, China.

出版信息

Sci Rep. 2017 Jun 6;7(1):2832. doi: 10.1038/s41598-017-02982-9.

DOI:10.1038/s41598-017-02982-9
PMID:28588267
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5460190/
Abstract

Reprogramming of adult somatic cells into induced pluripotent stem cells holds great promise in clinical therapy. Increasing evidences have shown that p53 and its target genes play important roles in somatic cell reprogramming. In this study, we report that PHLDA3, a p53 target gene, functions as a blockage of iPSCs generation by activating the Akt-GSK3β pathway. Furthermore, PHLDA3 is found to be transcriptionally regulated by Oct4. These findings reveal that PHLDA3 acts as a new member of the regulatory network of somatic cell reprogramming.

摘要

将成体体细胞重编程为诱导多能干细胞在临床治疗中具有巨大的应用前景。越来越多的证据表明,p53 及其靶基因在体细胞重编程中发挥着重要作用。在本研究中,我们报告了 p53 靶基因 PHLDA3 通过激活 Akt-GSK3β 通路来阻止 iPS 细胞的生成。此外,我们还发现 PHLDA3 的转录受到 Oct4 的调控。这些发现揭示了 PHLDA3 作为体细胞重编程调控网络的新成员发挥作用。

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C23 promotes tumorigenesis via suppressing p53 activity.C23通过抑制p53活性促进肿瘤发生。
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