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病毒劫持在神经发育病理学中的 Formins。

Viral Hijacking of Formins in Neurodevelopmental Pathologies.

机构信息

Department of Obstetrics, Gynecology and Reproductive Biology, College of Human Medicine, Michigan State University, MI, USA.

Department of Translational Science and Molecular Medicine, College of Human Medicine, Michigan State University, MI, USA.

出版信息

Trends Mol Med. 2017 Sep;23(9):778-785. doi: 10.1016/j.molmed.2017.07.004. Epub 2017 Aug 10.

Abstract

The 2015 Zika virus (ZIKV) outbreak caused global concern when it was determined to cause microcephaly, hearing loss, and other neurodevelopmental manifestations upon fetal exposure. Significant progress has been made in our understanding of the interactions between ZIKV and the pregnant host, but there is still a critical need to understand how ZIKV and other neurotropic viruses affect fetal neurodevelopment. Diaphanous-related formins (Diaphs) have recently been identified as microcephaly-associated proteins in humans and mice. Mutations in Diaphs affect the function of neural progenitor cells, much like prenatal viral infection. We present a novel hypothesis that viruses 'hijack' Diaphs in neural progenitor cells, causing autonomous differentiation and apoptosis of neural progenitor cells, which could potentially contribute to virus-associated neurological pathologies.

摘要

2015 年寨卡病毒(ZIKV)爆发引起了全球关注,因为它被确定会在胎儿暴露时导致小头畸形、听力损失和其他神经发育表现。我们在理解 ZIKV 与孕妇宿主之间的相互作用方面取得了重大进展,但仍迫切需要了解 ZIKV 和其他神经营养性病毒如何影响胎儿的神经发育。最近发现,神经管相关形态发生因子(Diaphs)是人类和小鼠中小头畸形相关的蛋白。Diaphs 的突变会影响神经祖细胞的功能,这与产前病毒感染非常相似。我们提出了一个新的假设,即病毒“劫持”神经祖细胞中的 Diaphs,导致神经祖细胞自主分化和凋亡,这可能导致与病毒相关的神经病理学。

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