ArticleThe Journal of physiology2000
Molecular determinant for run-down of L-type Ca2+ channels localized in the carboxyl terminus of the 1C subunit.
Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 35 citations in OpenAlex.
- Article
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- Article
- Calpastatin domain L is a partial agonist of the calmodulin-binding site for channel activation in Cav1.2 Ca2+ channels.The Journal of biological chemistry · 2011Article
- Inhibition of recombinant L-type voltage-gated calcium channels by positive allosteric modulators of GABAA receptors.The Journal of pharmacology and experimental therapeutics · 2011Article
- beta3-adrenergic receptor activation increases human atrial tissue contractility and stimulates the L-type Ca2+ current.The Journal of clinical investigation · 2008Article
- Atypical properties of a conventional calcium channel beta subunit from the platyhelminth Schistosoma mansoni.BMC physiology · 2008Article
- Atherosclerosis-related molecular alteration of the human CaV1.2 calcium channel alpha1C subunit.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Atrial fibrillation: basic mechanisms, remodeling and triggers.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2005Review
- Modulation of the voltage sensor of L-type Ca2+ channels by intracellular Ca2+.The Journal of general physiology · 2004Article
- Slow deactivation and U-shaped inactivation properties in cloned Cav1.2b channels in Chinese hamster ovary cells.Biophysical journal · 2003Article
- Mechanosensitivity of N-type calcium channel currents.Biophysical journal · 2002Article
- Functional diversity in neuronal voltage-gated calcium channels by alternative splicing of Ca(v)alpha1.Molecular neurobiology · 2002Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
1. The role of the sequence 1572-1651 in the C-terminal tail of the alpha1C subunit in run-down of Ca2+ channels was studied by comparing functional properties of the conventional alpha1C,77 channel with those of three isoforms carrying alterations in this motif. 2. The pore-forming alpha1C subunits were co-expressed with alpha2delta and beta2a subunits in HEK-tsA201 cells, a subclone of the human embryonic kidney cell line, and studied by whole-cell and single-channel patch-clamp techniques. 3. Replacement of amino acids 1572-1651 in alpha1C,77 with 81 different amino acids leading to alpha1C,86 significantly altered run-down behaviour. Run-down of Ba2+ currents was rapid with alpha1C,77 channels, but was slow with alpha1C,86. 4. Transfer of the alpha1C,86 segments L (amino acids 1572-1598) or K (amino acids 1595-1652) into the alpha1C,77 channel yielded alpha1C,77L and alpha1C,77K channels, respectively, the run-down of which resembled more that of alpha1C,77. These results demonstrate that a large stretch of sequence between residues 1572 and 1652 of alpha1C,86 renders Ca2+ channels markedly resistant to run-down. 5. The protease inhibitor calpastatin added together with ATP was able to reverse the run-down of alpha1C,77 channels. Calpastatin expression was demonstrated in the HEK-tsA cells by Western blot analysis. 6. These results indicate a significant role of the C-terminal sequence 1572-1651 of the alpha1C subunit in run-down of L-type Ca2+ channels and suggest this sequence as a target site for a modulatory effect by endogenous calpastatin.
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