Clarification of novel regulatory mechanism of intercellular junction in renal tubules

紧密连接将相邻的上皮细胞封闭在一个狭窄的带内，组成一个大型的蛋白质复合体，包括跨膜蛋白、支架蛋白和转录蛋白。Claudins是四跨蛋白，由20多个同源异构体组成的超家族。克拉丁的不同组合可以赋予上皮细胞不同的特性。然而，Claudins表达的调控机制在很大程度上仍不清楚。我们研究了Claudins在肾小管中表达的调控机制，发现了Claudin-2和Claudin-4的新转录机制，以及Claudin-16的细胞内转运机制。此外，我们还阐明了claudin-2和-4在抗高渗胁迫中的新功能。

Tight junctions, which seal adjacent epithelial cells in a narrow band, composes a large complex of proteins including transmembrane, scaffolding, and transcriptional proteins. Claudins are tetraspanning proteins and comprise a superfamily of more than 20 homologus isoforms. Different combinations of claudins can confer different properties to epithelial cells. However, the regulatory mechanisms of claudins expression remain largely unknown. We investigated the regulatory mechanisms of claudins expression in the renal tubule and found the novel transcriptional mechanism of claudin-2 and -4, and intracellular trafficking mechanism of claudin-16. Furthermore, we clarified the novel function of claudin-2 and -4 against hyperosmotic stress.