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在小鼠中删除p63外因子13揭示了在上皮细胞发育中的C端异型特异性功能

Anna Maria Lena¹, Artem Smirnov^1,2, Mara Mancini¹

¹Department of Experimental Medicine, University of Rome "Tor Vergata", Rome 00133, Italy.

Proceedings of the National Academy of Sciences of the United States of America

|July 17, 2025

概括

这是一种p63蛋白质.

科学领域:

发展生物学发展生物学
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

转录因子p63对于上皮细胞发育至关重要.
p63的3'UTR的替代拼接产生了不同的C端异型 (α,β,γ).
在p63的C端突变与AEC综合征有关.

研究的目的:

为了研究p63 C-终端的体内作用.
描述p63异型之间的功能差异.
了解p63相关的上皮缺陷背后的分子机制.

主要方法:

在表达氨酸-14的组织中产生了p63外因子13删除的小鼠模型.
利用转录组,全基因组占用率和互动组研究.
分析了p63蛋白表达和异型特异性功能.

主要成果:

小鼠模型主要表达了p63β异型,而不是p63α异型.
p63β与转录机制的相互作用增加,导致基因表达的改变.
细胞外基因基因的失调导致异常的角质细胞粘附,全身炎症和发育异常.

结论:

全长的ΔNp63α异型在上皮细胞发育中起着至关重要的作用,不能被β或γ异型替代.
p63α对于编排基因表达程序来进行适当的上皮质形成至关重要.
在维护上皮质完整性和预防发育缺陷方面,p63 C端起着至关重要的作用.

关键词:

SAM 域名是 SAM 的域名.粘附性粘附性粘附性粘附性增强剂是一种增强剂.在p63中,p63是什么?的 ΔNp63 的值.

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