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p53 将肿瘤发生与重编程连接到多能性。

p53 connects tumorigenesis and reprogramming to pluripotency.

机构信息

Department of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Münster 48149, Germany.

出版信息

J Exp Med. 2010 Sep 27;207(10):2045-8. doi: 10.1084/jem.20101866.

Abstract

The tumor suppressor gene p53 prevents the initiation of tumor formation by inducing cell cycle arrest, senescence, DNA repair, and apoptosis. Recently, the absence or mutation of p53 was described to facilitate nuclear reprogramming. These findings suggest an influence of p53 on the de-differentiation process, and highlight the similarities between induction of pluripotency and tumor formation.

摘要

抑癌基因 p53 通过诱导细胞周期停滞、衰老、DNA 修复和细胞凋亡来阻止肿瘤的发生。最近的研究表明,p53 的缺失或突变可促进核重编程。这些发现表明 p53 对去分化过程有影响,并突出了诱导多能性和肿瘤形成之间的相似性。

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