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Updated: Jan 13, 2026

Author Spotlight: Developing Parmodulins to Target Protease-Activated Receptors for Inflammation Control

Author Spotlight: Developing Parmodulins to Target Protease-Activated Receptors for Inflammation Control

Published on: May 24, 2024

上皮ナトリウムチャネル（ENaC）のP2Y2/PLC/PI(4,5)P2経路による調節に関する現在の理解

Tarek Mohamed Abd El-Aziz¹, Ahmed Al-Sabi², Lucia A Seale³

¹Zoology Department, Faculty of Science, Minia University, El-Minia, Egypt.

Purinergic signalling

|January 7, 2026

Abstract:

The epithelial sodium channel (ENaC) localized in the cell membrane is crucial for sodium transport and blood pressure regulation. Discovered in frog skin, ENaC is expressed in the colon, lungs, exocrine glands, and most notably in the distal nephron of the kidneys, where it limits sodium reabsorption. Mutations in ENaC cause hereditary hypertension (Liddle's syndrome) or hypotension (pseudohypoaldosteronism type 1). ENaC activity and expression are tightly controlled by various signaling molecules and second messengers. For example, urinary ATP binding to the P2Y2 receptor inhibits ENaC. ENaC also interacts with PI(4,5)P2 and the ubiquitin ligase Nedd4-2 via specific motifs. PI(4,5)P2 is essential for ENaC stability, trafficking, and gating. This review focuses on the regulatory roles of the P2Y2 receptor and PI(4,5)P2 on ENaC regulation.

キーワード:

上皮ナトリウムチャネルリン脂質プリン受容体

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