Inhibition of prostasin-induced ENaC activities by PN-1 and regulation of PN-1 expression by TGF-beta1 and aldosterone.

@article{Wakida2006InhibitionOP,
  title={Inhibition of prostasin-induced ENaC activities by PN-1 and regulation of PN-1 expression by TGF-beta1 and aldosterone.},
  author={Naoki Wakida and Kenichiro Kitamura and Do Gia Tuyen and Ai Maekawa and Taku Miyoshi and Masataka Adachi and N. Shiraishi and Takehiro Ko and Vu Ha and Hiroshi Nonoguchi and Kimio Tomita},
  journal={Kidney international},
  year={2006},
  volume={70 8},
  pages={1432-8}
}
Prostasin has been shown to regulate sodium handling in the kidney. Recently, a serine protease inhibitor, protease nexin-1 (PN-1), was identified as an endogenous inhibitor for prostasin. Therefore, we hypothesized that PN-1 may regulate sodium reabsorption by reducing prostasin activity, and that expression of PN-1 was regulated by transforming growth factor-beta1 (TGF-beta1) or aldosterone, like prostasin. cRNAs for epithelial sodium channel (ENaC), prostasin, and PN-1 were expressed in… CONTINUE READING

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