ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Switching of Ca2+-dependent inactivation of Ca(v)1.3 channels by calcium binding proteins of 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 115 papers.
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Who cites it
115 citing papers in PubMed, 155 citations in OpenAlex.
- Calmodulin: The Essential Biological Regulator Self-Regulates Its Activity, Structure and Function.Biology · 2026Review
- Molecular basis for a CaThe Journal of biological chemistry · 2026Article
- Calmodulinopathy variants impair CaV1.3 and CaV2.1 regulation.The Journal of general physiology · 2026Article
- Noise-Induced Hearing Loss Enhances CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- CaBP1 and 2 enable sustained CaeLife · 2024Article
- Comprehensive Characterization of a Subfamily of CaeNeuro · 2024Article
- Letting the calcium flow.eLife · 2024Article
- Asymmetric contribution of a selectivity filter gate in triggering inactivation of CaV1.3 channels.The Journal of general physiology · 2024Article
- Calmodulin Mutations in Human Disease.Channels (Austin, Tex.) · 2023Review
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- Regulation of Presynaptic Calcium Channels.Advances in neurobiology · 2023Article
- Tau isoform-specific enhancement of L-type calcium current and augmentation of afterhyperpolarization in rat hippocampal neurons.Scientific reports · 2022Article
- The Relevance of Amyloid β-Calmodulin Complexation in Neurons and Brain Degeneration in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Article
- Presynaptic calcium channels: specialized control of synaptic neurotransmitter release.Nature reviews. Neuroscience · 2020Review
- RBP2 stabilizes slow Cav1.3 CaPflugers Archiv : European journal of physiology · 2020Article
- Calcium Sensors in Neuronal Function and Dysfunction.Cold Spring Harbor perspectives in biology · 2019Review
- Single-Channel Resolution of the Interaction between C-Terminal CaBiophysical journal · 2019Article
- Splicing of an automodulatory domain in CaThe Journal of general physiology · 2018Article
55 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca(V)1.3 channels comprise a vital subdivision of L-type Ca2+ channels: Ca(V)1.3 channels mediate neurotransmitter release from auditory inner hair cells (IHCs), pancreatic insulin secretion, and cardiac pacemaking. Fitting with these diverse roles, Ca(V)1.3 channels exhibit striking variability in their inactivation by intracellular Ca2+. IHCs show generally weak-to-absent Ca2+-dependent inactivation (CDI), potentially permitting audition of sustained sounds. In contrast, the strong CDI seen elsewhere likely provides critical negative feedback. Here, we explore this mysterious CDI malleability, particularly its comparative weakness in hair cells. At baseline, heterologously expressed Ca(V)1.3 channels exhibit intense CDI, wherein each lobe of calmodulin (CaM) contributes a distinct inactivation component. Because CaM-like molecules (bearing four recognizable but not necessarily functional Ca2+-binding EF hands) can perturb the Ca2+ response of molecules regulated by CaM, we asked whether such CaM-like entities could influence CDI. We find that CaM-like calcium-binding protein (CaBP) molecules are clearly expressed within the organ of Corti. In particular, the rare subtype CaBP4 is specific to IHCs, and CaBP4 proves capable of eliminating even the potent baseline CDI of Ca(V)1.3. CaBP4 thereby represents a plausible candidate for moderating CDI within IHCs.
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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.