Cav1.4alpha1 subunits can form slowly inactivating dihydropyridine-sensitive L-type Ca2+ channels lacking Ca2+-dependent inactivation

The neuronal L-type calcium channels (LTCCs) Cav1.2alpha1 and Cav1.3alpha1 are functionally distinct. Cav1.3alpha1 activates at lower voltages and inactivates more slowly than Cav1.2alpha1, making it suitable to support sustained L-type Ca2+ inward currents (ICa,L) and serve in pacemaker functions....

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Veröffentlicht in:	The Journal of neuroscience 2003-07, Vol.23 (14), p.6041-6049
Hauptverfasser:	Koschak, Alexandra, Reimer, Daniel, Walter, Doris, Hoda, Jean-Charles, Heinzle, Thomas, Grabner, Manfred, Striessnig, Jörg
Format:	Artikel
Sprache:	eng
Schlagworte:	3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester - pharmacology Amino Acid Sequence Barium - metabolism Calcium - metabolism Calcium - pharmacology Calcium Channel Agonists - pharmacology Calcium Channel Blockers - pharmacology Calcium Channels Calcium Channels, L-Type - drug effects Calcium Channels, L-Type - genetics Calcium Channels, L-Type - metabolism Cell Line Cloning, Molecular Dihydropyridines - pharmacology Humans Ion Channel Gating - drug effects Ion Channel Gating - physiology Isradipine - pharmacology Kidney - cytology Kidney - metabolism Molecular Sequence Data Patch-Clamp Techniques Protein Subunits - drug effects Protein Subunits - genetics Protein Subunits - metabolism Sequence Homology, Amino Acid Transfection
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