ArticleThe Journal of physiology2006
Alternative splicing in the C-terminus of CaV2.2 controls expression and gating of N-type calcium channels.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 81 citations in OpenAlex.
- Article
- Spared but Not Silent: Ion Channel Plasticity in Uninjured Sensory Neurons in Neuropathic Pain.International journal of molecular sciences · 2026Review
- Synaptic Ca2+ channels and neurexins are linked through direct and indirect binding complexes.Scientific reports · 2026Article
- Voltage-Gated Ion Channels in Neuropathic Pain Signaling.Life (Basel, Switzerland) · 2025Review
- Calcium channel-coupled transcription factors facilitate direct nuclear signaling.Research square · 2025Article
- The intracellular C-terminus confers compartment-specific targeting of voltage-gated calcium channels.Cell reports · 2024Article
- Peptide and Peptidomimetic Inhibitors Targeting the Interaction of Collapsin Response Mediator Protein 2 with the N-Type Calcium Channel for Pain Relief.ACS pharmacology & translational science · 2024Review
- Clinical features and genetic analysis of developmental and epileptic encephalopathy caused by biallelic variants ofHeliyon · 2024Article
- The Interplay Between Splicing of Two Exon Combinations Differentially Affects Membrane Targeting and Function of Human CaFunction (Oxford, England) · 2024Article
- Epigenetic control of ion channel expression and cell-specific splicing in nociceptors: Chronic pain mechanisms and potential therapeutic targets.Channels (Austin, Tex.) · 2021Review
- Heat But Not Mechanical Hypersensitivity Depends on Voltage-Gated CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Constitutive activity of dopamine receptor type 1 (D1R) increases CaV2.2 currents in PFC neurons.The Journal of general physiology · 2020Article
- Article
- Cacna1b alternative splicing impacts excitatory neurotransmission and is linked to behavioral responses to aversive stimuli.Molecular brain · 2019Article
- Mechanisms of Neuronal Alternative Splicing and Strategies for Therapeutic Interventions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Review
- Article
- Calcium channel modulation as a target in chronic pain control.British journal of pharmacology · 2018Review
- Article
- The CaScientific reports · 2018Article
- Voltage-gated calcium channel αF1000Research · 2018Review
Corrections and comments
- Commented on by
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
N-type Ca(V)2.2 calcium channels localize to presynaptic nerve terminals of nociceptors where they control neurotransmitter release. Nociceptive neurons express a unique set of ion channels and receptors important for optimizing their role in transmission of noxious stimuli. Included among these is a structurally and functionally distinct N-type calcium channel splice isoform, Ca(V)2.2e[37a], expressed in a subset of nociceptors and with limited expression in other parts of the nervous system. Ca(V)2.2[e37a] arises from the mutually exclusive replacement of e37a for e37b in the C-terminus of Ca(V)2.2 mRNA. N-type current densities in nociceptors that express a combination of Ca(V)2.2e[37a] and Ca(V)2.2e[37b] mRNAs are significantly larger compared to cells that express only Ca(V)2.2e[37b]. Here we show that e37a supports increased expression of functional N-type channels and an increase in channel open time as compared to Ca(V)2.2 channels that contain e37b. To understand how e37a affects N-type currents we compared macroscopic and single-channel ionic currents as well as gating currents in tsA201 cells expressing Ca(V)2.2e[37a] and Ca(V)2.2e[37b]. When activated, Ca(V)2.2e[37a] channels remain open for longer and are expressed at higher density than Ca(V)2.2e[37b] channels. These unique features of the Ca(V)2.2e[37a] isoform combine to augment substantially the amount of calcium that enters cells in response to action potentials. Our studies of the e37a/e37b splice site reveal a multifunctional domain in the C-terminus of Ca(V)2.2 that regulates the overall activity of N-type calcium channels in nociceptors.
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.