Na(+) Entry and Modulation of Na(+)/Ca(2+) Exchange As a Key Mechanism of TRPC Signaling

Overview

Journal Pflugers Arch

Specialty Physiology

Date 2005 Jun 1

PMID 15924237

Citations 27

Authors

Petra Eder

Michael Poteser

Christoph Romanin

Klaus Groschner

Affiliations

Soon will be listed here.

Abstract

Ion channels formed by canonical transient receptor potential (TRPC) proteins are considered to be key players in cellular Ca(2+) homeostasis. As permeation of Ca(2+) through TRPC homo- and/or heteromeric channels has been repeatedly demonstrated, analysis of the physiological role of TRPC proteins was so far based on the concept that these proteins form regulated Ca(2+) entry channels. The well-recognized lack of cation selectivity of TRPC channels and the ability to generate substantial monovalent conductances that govern membrane potential and cation gradients were barely appreciated as a physiologically relevant issue. Nonetheless, recent studies suggest monovalent, specifically Na(+) permeation through TRPC cation channels as an important event in TRPC signaling. TRPC-mediated Na(+) entry may be converted into a distinct pattern of cellular Ca(2+) signals by interaction with Na(+)/Ca(2+) exchanger proteins. This review discusses current concepts regarding the link between Na(+) entry through TRPC channels and cellular Ca(2+) signaling.

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