Vangl as a Master Scaffold for Wnt/Planar Cell Polarity Signaling in Development and Disease.
Vangl as a Master Scaffold for Wnt/Planar Cell Polarity Signaling in Development and Disease.
复制标题
Vangl作为WNT/Planar细胞极性信号传导的主要支架。
DOI：
10.3389/fcell.2022.887100
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发表时间：
2022
影响因子：
5.5
通讯作者：
中科院分区：
文献类型：
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作者：
组织内极性的建立和动态的细胞形态发生事件是发育和成年组织的共同特征，这些程序的破坏与各种人类疾病有关。Wnt/平面细胞极性（Wnt/PCP）信号是非规范Wnt信号的一个分支，对上皮组织极性的建立和维持以及对胚胎正常发育至关重要的细胞运动事件至关重要。在上皮组织中，Wnt/ pcp介导的平面极性依赖于核心蛋白的不对称分布来建立极性，但Wnt/ pcp介导的细胞运动对这种分布的要求尚不清楚。然而，在极化组织和迁移细胞中，Wnt/PCP特异性跨膜蛋白Vangl是必需的，并且似乎作为一个支架，核心途径组分以及Wnt/PCP信号的正、负调节因子在其上组装。目前的文献表明，Vangl的多个相互作用域允许结合不同的信号伙伴，以建立上下文和组织特异性复合物。在这篇综述中，我们讨论了在发育和成人组织上皮组织极性和细胞运动事件中，Vangl作为Wnt/PCP信号传导的主支架的作用，以及这些程序在人类疾病中是如何失调的。
The establishment of polarity within tissues and dynamic cellular morphogenetic events are features common to both developing and adult tissues, and breakdown of these programs is associated with diverse human diseases. Wnt/Planar cell polarity (Wnt/PCP) signaling, a branch of non-canonical Wnt signaling, is critical to the establishment and maintenance of polarity in epithelial tissues as well as cell motility events critical to proper embryonic development. In epithelial tissues, Wnt/PCP-mediated planar polarity relies upon the asymmetric distribution of core proteins to establish polarity, but the requirement for this distribution in Wnt/PCP-mediated cell motility remains unclear. However, in both polarized tissues and migratory cells, the Wnt/PCP-specific transmembrane protein Vangl is required and appears to serve as a scaffold upon which the core pathway components as well as positive and negative regulators of Wnt/PCP signaling assemble. The current literature suggests that the multiple interaction domains of Vangl allow for the binding of diverse signaling partners for the establishment of context- and tissue-specific complexes. In this review we discuss the role of Vangl as a master scaffold for Wnt/PCP signaling in epithelial tissue polarity and cellular motility events in developing and adult tissues, and address how these programs are dysregulated in human disease.