ArticleThe Journal of general physiology1997
Structural regions of the cardiac Ca channel alpha subunit involved in Ca-dependent inactivation.
Article in The Journal of general physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Calcium channel gating.Pflugers Archiv : European journal of physiology · 2018Review
- Key role of segment IS4 in Cav1.2 inactivation: link between activation and inactivation.Pflugers Archiv : European journal of physiology · 2017Article
- Localized calcineurin confers Ca2+-dependent inactivation on neuronal L-type Ca2+ channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- The ß subunit of voltage-gated Ca2+ channels.Physiological reviews · 2010Review
- CaV1.2 channelopathies: from arrhythmias to autism, bipolar disorder, and immunodeficiency.Pflugers Archiv : European journal of physiology · 2010Review
- Sequence differences in the IQ motifs of CaV1.1 and CaV1.2 strongly impact calmodulin binding and calcium-dependent inactivation.The Journal of biological chemistry · 2008Article
- The Timothy syndrome mutation differentially affects voltage- and calcium-dependent inactivation of CaV1.2 L-type calcium channels.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Physiological modulation of inactivation in L-type Ca2+ channels: one switch.The Journal of physiology · 2004Review
- Apocalmodulin and Ca2+ calmodulin-binding sites on the CaV1.2 channel.Biophysical journal · 2003Article
- Reconstituted slow muscarinic inhibition of neuronal (Ca(v)1.2c) L-type Ca2+ channels.Biophysical journal · 2002Article
- Proteolytic modification of swelling-activated Cl- current in LNCaP prostate cancer epithelial cells.Journal of bioenergetics and biomembranes · 2002Article
- Alternatively spliced alpha(1G) (Ca(V)3.1) intracellular loops promote specific T-type Ca(2+) channel gating properties.Biophysical journal · 2001Article
- Molecular determinants of inactivation within the I-II linker of alpha1E (CaV2.3) calcium channels.Biophysical journal · 2001Article
- The [beta]2a subunit is a molecular groom for the Ca2+ channel inactivation gate.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Molecular determinants of inactivation in voltage-gated Ca2+ channels.The Journal of physiology · 2000Review
- Critical determinants of Ca(2+)-dependent inactivation within an EF-hand motif of L-type Ca(2+) channels.Biophysical journal · 2000Article
- Voltage- and calcium-dependent inactivation of calcium channels in Lymnaea neurons.The Journal of general physiology · 1999Article
- Kinetics of inactivation and restoration from inactivation of the L-type calcium current in human myotubes.The Journal of physiology · 1999Article
- Mutations in the EF-hand motif impair the inactivation of barium currents of the cardiac alpha1C channel.Biophysical journal · 1998Article
- Ca2+-sensitive inactivation of L-type Ca2+ channels depends on multiple cytoplasmic amino acid sequences of the alpha1C subunit.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
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2 authors.
Funding
Abstract
We investigated the molecular basis for Ca-dependent inactivation of the cardiac L-type Ca channel. Transfection of HEK293 cells with the wild-type alpha or its 3' deletion mutant (alpha) produced channels that exhibited prominent Ca-dependent inactivation. To identify structural regions of alpha involved in this process, we analyzed chimeric alpha subunits in which one of the major intracellular domains of alpha was replaced by the corresponding region from the skeletal muscle alpha subunit (which lacks Ca-dependent inactivation). Replacing the NH terminus or the III-IV loop of alpha with its counterpart from alpha had no appreciable effect on Ca channel inactivation. In contrast, replacing the I-II loop of alpha with the corresponding region from alpha dramatically slowed the inactivation of Ba currents while preserving Ca-dependent inactivation. A similar but less pronounced result was obtained with a II-III loop chimera. These results suggest that the I-II and II-III loops of alpha may participate in the mechanism of Ca-dependent inactivation. Replacing the final 80% of the COOH terminus of alpha with the corresponding region from alpha completely eliminated Ca-dependent inactivation without affecting inactivation of Ba currents. Significantly, Ca-dependent inactivation was restored to this chimera by deleting a nonconserved, 211-amino acid segment from the end of the COOH terminus. These results suggest that the distal COOH terminus of alpha can block Ca-dependent inactivation, possibly by interacting with other proteins or other regions of the Ca channel. Our findings suggest that structural determinants of Ca-dependent inactivation are distributed among several major cytoplasmic domains of alpha.
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