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首页> 外文期刊>Molecular and Cellular Biology >The Rho Target PRK2 Regulates Apical Junction Formation in Human Bronchial Epithelial Cells
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The Rho Target PRK2 Regulates Apical Junction Formation in Human Bronchial Epithelial Cells

机译：Rho靶标PRK2调节人支气管上皮细胞顶尖结的形成。

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Rho GTPases regulate multiple signaling pathways to control a number of cellular processes during epithelial morphogenesis. To investigate the downstream pathways through which Rho regulates epithelial apical junction formation, we screened a small interfering RNA (siRNA) library targeting 28 known Rho target proteins in 16HBE human bronchial epithelial cells. This led to the identification of the serine-threonine kinase PRK2 (protein kinase C-related kinase 2, also called PKN2). Depletion of PRK2 does not block the initial formation of primordial junctions at nascent cell-cell contacts but does prevent their maturation into apical junctions. PRK2 is recruited to primordial junctions, and this localization depends on its C2-like domain. Rho binding is essential for PRK2 function and also facilitates PRK2 recruitment to junctions. Kinase-dead PRK2 acts as a dominant-negative mutant and prevents apical junction formation. We conclude that PRK2 is recruited to nascent cell-cell contacts through its C2-like and Rho-binding domains and promotes junctional maturation through a kinase-dependent pathway.
机译：Rho GTPases调节多种信号传导途径，以控制上皮形态发生过程中的许多细胞过程。为了研究Rho调节上皮顶部连接形成的下游途径，我们在16HBE人支气管上皮细胞中筛选了针对28种已知Rho靶蛋白的小干扰RNA（siRNA）文库。这导致了丝氨酸-苏氨酸激酶PRK2（蛋白激酶C相关激酶2，也称为PKN2）的鉴定。 PRK2的消耗不会阻止新生细胞间接触时原始连接的最初形成，但会阻止其成熟成顶端连接。 PRK2被募集到原始连接处，并且该定位取决于其C2样结构域。 Rho结合对于PRK2功能至关重要，也有助于PRK2募集到结。激酶死亡的PRK2作为显性负突变体，可防止根尖连接的形成。我们得出的结论是PRK2通过其C2样和Rho结合域被募集到新生的细胞间接触，并通过激酶依赖性途径促进连接成熟。

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