Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
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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- Führende Autor*innen der Med Uni Graz
- Groschner Klaus
- Co-Autor*innen der 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