ArticleJournal of molecular biology2013
Apo states of calmodulin and CaBP1 control CaV1 voltage-gated calcium channel function through direct competition for the IQ domain.
Article in Journal of molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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.
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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
39 citing papers in PubMed, 53 citations in OpenAlex.
- Structural Insights into L-Type Voltage-Gated CaBiochemistry · 2026Article
- Structure-Function Diversity of Calcium-Binding Proteins (CaBPs): Key Roles in Cell Signalling and Disease.Cells · 2025Review
- Caldendrin Is a Repressor of PIEZO2 Channels and Touch Sensation in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- Regulation of Presynaptic Calcium Channels.Advances in neurobiology · 2023Article
- Chemical shift assignments of calmodulin under standard conditions at neutral pH.Biomolecular NMR assignments · 2022Article
- Chemical shift assignments of the C-terminal domain of CaBP1 bound to the IQ-motif of voltage-gated CaBiomolecular NMR assignments · 2022Article
- L-Type CaBiomolecules · 2021Review
- NaStructure (London, England : 1993) · 2021Article
- CaThe Journal of biological chemistry · 2020Article
- α-Actinin-1 promotes activity of the L-type CaThe EMBO journal · 2020Article
- RBP2 stabilizes slow Cav1.3 CaPflugers Archiv : European journal of physiology · 2020Article
- The S2-S3 Loop of Kv7.4 Channels Is Essential for Calmodulin Regulation of Channel Activation.Frontiers in physiology · 2020Article
- Crystal structures of CaProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Calcium Sensors in Neuronal Function and Dysfunction.Cold Spring Harbor perspectives in biology · 2019Review
- Caldendrin and Calneurons-EF-Hand CaM-Like Calcium Sensors With Unique Features and Specialized Neuronal Functions.Frontiers in molecular neuroscience · 2019Review
- Splicing of an automodulatory domain in CaThe Journal of general physiology · 2018Article
- 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
- A Calmodulin C-Lobe CaNeuron · 2018Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
In neurons, binding of calmodulin (CaM) or calcium-binding protein 1 (CaBP1) to the CaV1 (L-type) voltage-gated calcium channel IQ domain endows the channel with diametrically opposed properties. CaM causes calcium-dependent inactivation and limits calcium entry, whereas CaBP1 blocks calcium-dependent inactivation (CDI) and allows sustained calcium influx. Here, we combine isothermal titration calorimetry with cell-based functional measurements and mathematical modeling to show that these calcium sensors behave in a competitive manner that is explained quantitatively by their apo-state binding affinities for the IQ domain. This competition can be completely blocked by covalent tethering of CaM to the channel. Further, we show that Ca(2+)/CaM has a sub-picomolar affinity for the IQ domain that is achieved without drastic alteration of calcium-binding properties. The observation that the apo forms of CaM and CaBP1 compete with each other demonstrates a simple mechanism for direct modulation of CaV1 function and suggests a means by which excitable cells may dynamically tune CaV activity.
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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.