ArticleBiophysical journal2008
Role of N-terminal domain and accessory subunits in controlling deactivation-inactivation coupling of Kv4.2 channels.
Article in Biophysical journal, 2008. 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.
- KChIP1 splice variants modulate Kv4 channels by promoting P/C-type inactivation features.Scientific reports · 2026Article
- Etiological involvement of KCND1 variants in an X-linked neurodevelopmental disorder with variable expressivity.American journal of human genetics · 2024Article
- Article
- Kv channel-interacting proteins as neuronal and non-neuronal calcium sensors.Channels (Austin, Tex.) · 2018Review
- Article
- Modulation of human Kv4.3/KChIP2 channel inactivation kinetics by cytoplasmic CaPflugers Archiv : European journal of physiology · 2017Article
- β Subunits Functionally Differentiate Human Kv4.3 Potassium Channel Splice Variants.Frontiers in physiology · 2017Article
- Article
- Modeling-independent elucidation of inactivation pathways in recombinant and native A-type Kv channels.The Journal of general physiology · 2012Article
- Voltage sensor inactivation in potassium channels.Frontiers in pharmacology · 2012Article
- Cytoplasmic domains and voltage-dependent potassium channel gating.Frontiers in pharmacology · 2012Article
- Mechanisms of closed-state inactivation in voltage-gated ion channels.The Journal of physiology · 2011Review
- The dipeptidyl-peptidase-like protein DPP6 determines the unitary conductance of neuronal Kv4.2 channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- The domain and conformational organization in potassium voltage-gated ion channels.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2009Review
- Dynamic coupling of voltage sensor and gate involved in closed-state inactivation of kv4.2 channels.The Journal of general physiology · 2009Article
- Dynamic, nonlinear feedback regulation of slow pacemaking by A-type potassium current in ventral tegmental area neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- The neuronal Kv4 channel complex.Neurochemical research · 2008Review
- The "structurally minimal" isoform KChIP2d modulates recovery of K(v)4.3 N-terminal deletion mutant Δ2-39.Channels (Austin, Tex.)Review
- K(V)4.3 N-terminal deletion mutant Δ2-39: effects on inactivation and recovery characteristics in both the absence and presence of KChIP2b.Channels (Austin, Tex.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We examined the relationship between deactivation and inactivation in Kv4.2 channels. In particular, we were interested in the role of a Kv4.2 N-terminal domain and accessory subunits in controlling macroscopic gating kinetics and asked if the effects of N-terminal deletion and accessory subunit coexpression conform to a kinetic coupling of deactivation and inactivation. We expressed Kv4.2 wild-type channels and N-terminal deletion mutants in the absence and presence of Kv channel interacting proteins (KChIPs) and dipeptidyl aminopeptidase-like proteins (DPPs) in human embryonic kidney 293 cells. Kv4.2-mediated A-type currents at positive and deactivation tail currents at negative membrane potentials were recorded under whole-cell voltage-clamp and analyzed by multi-exponential fitting. The observed changes in Kv4.2 macroscopic inactivation kinetics caused by N-terminal deletion, accessory subunit coexpression, or a combination of the two maneuvers were compared with respective changes in deactivation kinetics. Extensive correlation analyses indicated that modulatory effects on deactivation closely parallel respective effects on inactivation, including both onset and recovery kinetics. Searching for the structural determinants, which control deactivation and inactivation, we found that in a Kv4.2 Delta 2-10 N-terminal deletion mutant both the initial rapid phase of macroscopic inactivation and tail current deactivation were slowed. On the other hand, the intermediate and slow phase of A-type current decay, recovery from inactivation, and tail current decay kinetics were accelerated in Kv4.2 Delta 2-10 by KChIP2 and DPPX. Thus, a Kv4.2 N-terminal domain, which may control both inactivation and deactivation, is not necessary for active modulation of current kinetics by accessory subunits. Our results further suggest distinct mechanisms for Kv4.2 gating modulation by KChIPs and DPPs.
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.