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Eder, P; Poteser, M; Romanin, C; Groschner, K.
Na(+) entry and modulation of Na(+)/Ca(2+) exchange as a key mechanism of TRPC signaling.
Pflugers Arch. 2005; 451(1):99-104 Doi: 10.1007/s00424-005-1434-2
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Leading authors Med Uni Graz: Groschner Klaus
Co-authors Med Uni Graz: Poteser Michael
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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.
Find related publications in this database (using NLM MeSH Indexing): Animals -; Calcium - metabolism; Calcium Signaling -; Humans -; Models, Biological -; Rats -; Signal Transduction - physiology; Sodium - metabolism; Sodium-Calcium Exchanger - physiology; TRPC Cation Channels - physiology
Find related publications in this database (Keywords): TRPC proteins; non-selective cation channels; Ca2+ signaling; Na+/Ca2+ exchange