ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Ca2+-binding protein-1 facilitates and forms a postsynaptic complex with Cav1.2 (L-type) Ca2+ channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
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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
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Calcium and arrhythmogenesis.Physiological reviews · 2007Pooled it
- 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
- Cholinergic regulation of dendritic CaProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Comprehensive Characterization of a Subfamily of CaeNeuro · 2024Article
- 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
- Caldendrin represses neurite regeneration and growth in dorsal root ganglion neurons.Scientific reports · 2023Article
- Calcium Channels in Retinal Function and Disease.Annual review of vision science · 2022Review
- L-Type CaBiomolecules · 2021Review
- 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
- CaNeuroscience · 2018Article
- CaBP1 regulates CaMolecular and cellular neurosciences · 2018Article
- Densin-180 Controls the Trafficking and Signaling of L-Type Voltage-Gated CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Characterization of C-terminal Splice Variants of Cav1.4 Ca2+ Channels in Human Retina.The Journal of biological chemistry · 2016Article
- Article
- Decalmodulation of Cav1 channels by CaBPs.Channels (Austin, Tex.) · 2016Review
- Sense and specificity in neuronal calcium signalling.Biochimica et biophysica acta · 2015Review
- The role of auxiliary subunits for the functional diversity of voltage-gated calcium channels.Journal of cellular physiology · 2015Review
9 more citing papers are in PubMed but not listed here.
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Ca2+-binding protein-1 (CaBP1) is a Ca2+-binding protein that is closely related to calmodulin (CaM) and localized in somatodendritic regions of principal neurons throughout the brain, but how CaBP1 participates in postsynaptic Ca2+ signaling is not known. Here, we describe a novel role for CaBP1 in the regulation of Ca2+ influx through Ca(v)1.2 (L-type) Ca2+ channels. CaBP1 interacts directly with the alpha1 subunit of Ca(v)1.2 at sites that also bind CaM. CaBP1 binding to one of these sites, the IQ domain, is Ca2+ dependent and competitive with CaM binding. The physiological significance of this interaction is supported by the association of Ca(v)1.2 and CaBP1 in postsynaptic density fractions purified from rat brain. Moreover, in double-label immunofluorescence experiments, CaBP1 and Ca(v)1.2 colocalize in numerous cell bodies and dendrites of neurons, particularly in pyramidal cells in the CA3 region of the hippocampus and in the dorsal cortex. In electrophysiological recordings of cells transfected with Ca(v)1.2, CaBP1 greatly prolonged Ca2+ currents, prevented Ca2+-dependent inactivation, and caused Ca2+-dependent facilitation of currents evoked by step depolarizations and repetitive stimuli. These effects contrast with those of CaM, which promoted strong Ca2+-dependent inactivation of Ca(v)1.2 with these same voltage protocols. Our findings reveal how Ca2+-binding proteins, such as CaM and CaBP1, differentially adjust Ca2+ influx through Ca(v)1.2 channels, which may specify diverse modes of Ca2+ signaling in neurons.
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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.