ArticleStructure (London, England : 1993)2010
Structural basis for the differential effects of CaBP1 and calmodulin on Ca(V)1.2 calcium-dependent inactivation.
Article in Structure (London, England : 1993), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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Who cites it
47 citing papers in PubMed, 69 citations in OpenAlex.
- Molecular basis for a CaThe Journal of biological chemistry · 2026Article
- Structural Insights into L-Type Voltage-Gated CaBiochemistry · 2026Article
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- Structure-Function Diversity of Calcium-Binding Proteins (CaBPs): Key Roles in Cell Signalling and Disease.Cells · 2025Review
- CaBP1 and 2 enable sustained CaeLife · 2024Article
- Comprehensive Characterization of a Subfamily of CaeNeuro · 2024Article
- Calcium-Associated Proteins in Neuroregeneration.Biomolecules · 2024Review
- 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
- 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
- Solid-State NMR Study to Probe the Effects of Divalent Metal Ions (CaLangmuir : the ACS journal of surfaces and colloids · 2021Article
- 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
- Voltage-Gated Calcium Channels: Key Players in Sensory Coding in the Retina and the Inner Ear.Physiological reviews · 2018Review
- Allosteric regulators selectively prevent CaeLife · 2018Article
- CaNeuroscience · 2018Article
- Alternative Splicing at N Terminus and Domain I Modulates CaBiophysical journal · 2018Article
- Lead poisoning: acute exposure of the heart to lead ions promotes changes in cardiac function and Cav1.2 ion channels.Biophysical reviews · 2017Review
- CaProceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Calcium-binding protein 1 (CaBP1), a calmodulin (CaM) homolog, endows certain voltage-gated calcium channels (Ca(V)s) with unusual properties. CaBP1 inhibits Ca(V)1.2 calcium-dependent inactivation (CDI) and introduces calcium-dependent facilitation (CDF). Here, we show that the ability of CaBP1 to inhibit Ca(V)1.2 CDI and induce CDF arises from interaction between the CaBP1 N-lobe and interlobe linker residue Glu94. Unlike CaM, where functional EF hands are essential for channel modulation, CDI inhibition does not require functional CaBP1 EF hands. Furthermore, CaBP1-mediated CDF has different molecular requirements than CaM-mediated CDF. Overall, the data show that CaBP1 comprises two structural modules having separate functions: similar to CaM, the CaBP1 C-lobe serves as a high-affinity anchor that binds the Ca(V)1.2 IQ domain at a site that overlaps with the Ca²+/CaM C-lobe site, whereas the N-lobe/linker module houses the elements required for channel modulation. Discovery of this division provides the framework for understanding how CaBP1 regulates Ca(V)s.
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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.