PHLDA3 impedes somatic cell reprogramming by activating Akt-GSK3β pathway.
PHLDA3 impedes somatic cell reprogramming by activating Akt-GSK3β pathway.
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PHLDA3 通过激活 Akt-GSK3 β 途径阻碍体细胞重编程
DOI：
10.1038/s41598-017-02982-9
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发表时间：
2017-06-06
影响因子：
4.6
通讯作者：
Hu W
中科院分区：
文献类型：
--
作者：
Qiao M;Wu M;Shi R;Hu W
将成体细胞重编程为诱导多能干细胞在临床治疗中具有很大的前景。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重要作用。在这项研究中，我们报告了PHLDA 3，一个p53靶基因，通过激活Akt-GSK 3 β途径阻断iPSCs的产生。此外，PHLDA 3被发现是转录调节Oct 4。这些发现揭示了PHLDA 3作为体细胞重编程调控网络的新成员。
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.