ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Alternative splicing of the Ca(v)1.3 channel IQ domain, a molecular switch for Ca2+-dependent inactivation within auditory hair cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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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.
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Who cites it
48 citing papers in PubMed.
- Noise-Induced Hearing Loss Enhances CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Diversity matters - extending sound intensity coding by inner hair cells via heterogeneous synapses.The EMBO journal · 2023Review
- Alternative splicing in shaping the molecular landscape of the cochlea.Frontiers in cell and developmental biology · 2023Review
- Inhibition of a transcriptional repressor rescues hearing in a splicing factor-deficient mouse.Life science alliance · 2020Article
- Presynaptic calcium channels: specialized control of synaptic neurotransmitter release.Nature reviews. Neuroscience · 2020Review
- A Selectivity Filter Gate Controls Voltage-Gated Calcium Channel Calcium-Dependent Inactivation.Neuron · 2019Article
- Voltage-Gated Calcium Channels: Key Players in Sensory Coding in the Retina and the Inner Ear.Physiological reviews · 2018Review
- CaBP1 regulates CaMolecular and cellular neurosciences · 2018Article
- New gain-of-function mutation shows CACNA1D as recurrently mutated gene in autism spectrum disorders and epilepsy.Human molecular genetics · 2017Article
- CaProceedings of the National Academy of Sciences of the United States of America · 2017Article
- CaThe Journal of physiology · 2016Review
- An autism-associated mutation in CaV1.3 channels has opposing effects on voltage- and Ca(2+)-dependent regulation.Scientific reports · 2016Article
- Post-transcriptional modifications and "Calmodulation" of voltage-gated calcium channel function: Reflections by two collaborators of David T Yue.Channels (Austin, Tex.) · 2016Review
- Decalmodulation of Cav1 channels by CaBPs.Channels (Austin, Tex.) · 2016Review
- The emerging role of RNA editing in plasticity.The Journal of experimental biology · 2015Review
- Regulation of Ion Channel and Transporter Function Through RNA Editing.Current issues in molecular biology · 2015Review
- Towards a Unified Theory of Calmodulin Regulation (Calmodulation) of Voltage-Gated Calcium and Sodium Channels.Current molecular pharmacology · 2015Review
- Voltage-Gated Cav1 Channels in Disorders of Vision and Hearing.Current molecular pharmacology · 2015Review
- More than a pore: ion channel signaling complexes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Review
- Calmodulin regulation (calmodulation) of voltage-gated calcium channels.The Journal of general physiology · 2014Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Native Ca(V)1.3 channels within cochlear hair cells exhibit a surprising lack of Ca2+-dependent inactivation (CDI), given that heterologously expressed Ca(V)1.3 channels show marked CDI. To determine whether alternative splicing at the C terminus of the Ca(V)1.3 gene may produce a hair cell splice variant with weak CDI, we transcript-scanned mRNA obtained from rat cochlea. We found that the alternate use of exon 41 acceptor sites generated a splice variant that lost the calmodulin-binding IQ motif of the C terminus. These Ca(V)1.3(IQdelta) ("IQ deleted") channels exhibited a lack of CDI, which was independent of the type of coexpressed beta-subunits. Ca(V)1.3(IQdelta) channel immunoreactivity was preferentially localized to cochlear outer hair cells (OHCs), whereas that of Ca(V)1.3(IQfull) channels (IQ-possessing) labeled inner hair cells (IHCs). The preferential expression of Ca(V)1.3(IQdelta) within OHCs suggests that these channels may play a role in processes such as electromotility or activity-dependent gene transcription rather than neurotransmitter release, which is performed predominantly by IHCs in the cochlea.
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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.