ArticleBiophysical journal2003
Two components of voltage-dependent inactivation in Ca(v)1.2 channels revealed by its gating currents.
Article in Biophysical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- CaBP1 and 2 enable sustained CaeLife · 2024Article
- Fifty years of gating currents and channel gating.The Journal of general physiology · 2023Review
- Bacterial toxins and heart function: heat-labileBiophysical reviews · 2023Article
- Models of the cardiac L-type calcium current: A quantitative review.WIREs mechanisms of disease · 2023Review
- Increased CaScientific reports · 2022Article
- How CaThe Journal of general physiology · 2019Article
- Lead poisoning: acute exposure of the heart to lead ions promotes changes in cardiac function and Cav1.2 ion channels.Biophysical reviews · 2017Review
- Sodium channel diversity in the vestibular ganglion: NaV1.5, NaV1.8, and tetrodotoxin-sensitive currents.Journal of neurophysiology · 2016Article
- Energy variational analysis of ions in water and channels: Field theory for primitive models of complex ionic fluids.The Journal of chemical physics · 2010Article
- Ahnak1 modulates L-type Ca(2+) channel inactivation of rodent cardiomyocytes.Pflugers Archiv : European journal of physiology · 2010Article
- Mutations of nonconserved residues within the calcium channel alpha1-interaction domain inhibit beta-subunit potentiation.The Journal of general physiology · 2008Article
- Roscovitine, a cyclin-dependent kinase inhibitor, affects several gating mechanisms to inhibit cardiac L-type (Ca(V)1.2) calcium channels.British journal of pharmacology · 2007Article
- Kinetic properties of the cardiac L-type Ca2+ channel and its role in myocyte electrophysiology: a theoretical investigation.Biophysical journal · 2007Article
- Role of extracellular Ca2+ in gating of CaV1.2 channels.The Journal of physiology · 2005Article
- FPL 64176 modification of Ca(V)1.2 L-type calcium channels: dissociation of effects on ionic current and gating current.Biophysical journal · 2005Article
- Negatively charged residues in the N-terminal of the AID helix confer slow voltage dependent inactivation gating to CaV1.2.Biophysical journal · 2004Article
- Modulation of the voltage sensor of L-type Ca2+ channels by intracellular Ca2+.The Journal of general physiology · 2004Article
- Two components of voltage-dependent inactivation in Ca(v)1.2 channels revealed by its gating currents.Biophysical journal · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Voltage-dependent inactivation (VDI) was studied through its effects on the voltage sensor in Ca(v)1.2 channels expressed in tsA 201 cells. Two kinetically distinct phases of VDI in onset and recovery suggest the presence of dual VDI processes. Upon increasing duration of conditioning depolarizations, the half-distribution potential (V(1/2)) of intramembranous mobile charge was negatively shifted as a sum of two exponential terms, with time constants 0.5 s and 4 s, and relative amplitudes near 50% each. This kinetics behavior was consistent with that of increment of maximal charge related to inactivation (Qn). Recovery from inactivation was also accompanied by a reduction of Qn that varied with recovery time as a sum of two exponentials. The amplitudes of corresponding exponential terms were strongly correlated in onset and recovery, indicating that channels recover rapidly from fast VDI and slowly from slow VDI. Similar to charge "immobilization," the charge moved in the repolarization (OFF) transient became slower during onset of fast VDI. Slow VDI had, instead, hallmarks of interconversion of charge. Confirming the mechanistic duality, fast VDI virtually disappeared when Li(+) carried the current. A nine-state model with parallel fast and slow inactivation pathways from the open state reproduces most of the observations.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.