ArticleThe Journal of general physiology2009
Different pathways for activation and deactivation in CaV1.2: a minimal gating model.
Article in The Journal of general physiology, 2009. 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.
- Article
- CaV1.2 channelopathic mutations evoke diverse pathophysiological mechanisms.The Journal of general physiology · 2022Article
- Permeabilizing Cell Membranes with Electric Fields.Cancers · 2021Review
- Calcium Channel Splice Variants and Their Effects in Brain and Cardiovascular Function.Advances in experimental medicine and biology · 2021Article
- Post-Translational Modification of Cav1.2 and its Role in Neurodegenerative Diseases.Frontiers in pharmacology · 2021Review
- 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
- Upward movement of IS4 and IIIS4 is a rate-limiting stage in CaPflugers Archiv : European journal of physiology · 2016Article
- Functional heterogeneity of the four voltage sensors of a human L-type calcium channel.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Methods for quantification of pore-voltage sensor interaction in Ca(V)1.2.Pflugers Archiv : European journal of physiology · 2014Article
- Neutralisation of a single voltage sensor affects gating determinants in all four pore-forming S6 segments of Ca(V)1.2: a cooperative gating model.Pflugers Archiv : European journal of physiology · 2012Article
- Physicochemical properties of pore residues predict activation gating of Ca V1.2: a correlation mutation analysis.Pflugers Archiv : European journal of physiology · 2011Article
- Molecular endpoints of Ca2+/calmodulin- and voltage-dependent inactivation of Ca(v)1.3 channels.The Journal of general physiology · 2010Article
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6 authors.
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Abstract
Point mutations in pore-lining S6 segments of CaV1.2 shift the voltage dependence of activation into the hyperpolarizing direction and significantly decelerate current activation and deactivation. Here, we analyze theses changes in channel gating in terms of a circular four-state model accounting for an activation R-A-O and a deactivation O-D-R pathway. Transitions between resting-closed (R) and activated-closed (A) states (rate constants x(V) and y(V)) and open (O) and deactivated-open (D) states (u(V) and w(V)) describe voltage-dependent sensor movements. Voltage-independent pore openings and closures during activation (A-O) and deactivation (D-R) are described by rate constants alpha and beta, and gamma and delta, respectively. Rate constants were determined for 16-channel constructs assuming that pore mutations in IIS6 do not affect the activating transition of the voltage-sensing machinery (x(V) and y(V)). Estimated model parameters of 15 CaV1.2 constructs well describe the activation and deactivation processes. Voltage dependence of the "pore-releasing" sensor movement ((x(V)) was much weaker than the voltage dependence of "pore-locking" sensor movement (y(V)). Our data suggest that changes in membrane voltage are more efficient in closing than in opening CaV1.2. The model failed to reproduce current kinetics of mutation A780P that was, however, accurately fitted with individually adjusted x(V) and y(V). We speculate that structural changes induced by a proline substitution in this position may disturb the voltage-sensing domain.
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