ArticleNature chemical biology2014
Allostery in Ca²⁺ channel modulation by calcium-binding proteins.
Article in Nature chemical biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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
36 citing papers in PubMed, 55 citations in OpenAlex.
- Molecular basis for a CaThe Journal of biological chemistry · 2026Article
- Exploring the potential for gene therapy in Cav1.4-related retinal channelopathies.Channels (Austin, Tex.) · 2025Review
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- CaBP1 and 2 enable sustained CaeLife · 2024Article
- Probing ion channel macromolecular interactions using fluorescence resonance energy transfer.Methods in enzymology · 2021Article
- CaThe Journal of biological chemistry · 2020Article
- RBP2 stabilizes slow Cav1.3 CaPflugers Archiv : European journal of physiology · 2020Article
- Voltage- and calcium-gated ion channels of neurons in the vertebrate retina.Progress in retinal and eye research · 2019Review
- 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
- 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
- Duplex signaling by CaM and Stac3 enhances CaThe Journal of general physiology · 2018Article
- Synaptically silent sensory hair cells in zebrafish are recruited after damage.Nature communications · 2018Article
- CaBP1 regulates CaMolecular and cellular neurosciences · 2018Article
- Bilobal architecture is a requirement for calmodulin signaling to CaProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Channeling Vision: CaBioMed research international · 2018Review
- Calmodulin regulates CaThe Journal of biological chemistry · 2017Article
- Investigating State Restriction in Fluorescent Protein FRET Using Time-Resolved Fluorescence and Anisotropy.The journal of physical chemistry. C, Nanomaterials and interfaces · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Distinguishing between allostery and competition among modulating ligands is challenging for large target molecules. Out of practical necessity, inferences are often drawn from in vitro assays on target fragments, but such inferences may belie actual mechanisms. One key example of such ambiguity concerns calcium-binding proteins (CaBPs) that tune signaling molecules regulated by calmodulin (CaM). As CaBPs resemble CaM, CaBPs are believed to competitively replace CaM on targets. Yet, brain CaM expression far surpasses that of CaBPs, raising questions as to whether CaBPs can exert appreciable biological actions. Here, we devise a live-cell, holomolecule approach that reveals an allosteric mechanism for calcium channels whose CaM-mediated inactivation is eliminated by CaBP4. Our strategy is to covalently link CaM and/or CaBP to holochannels, enabling live-cell fluorescence resonance energy transfer assays to resolve a cyclical allosteric binding scheme for CaM and CaBP4 to channels, thus explaining how trace CaBPs prevail. This approach may apply generally for discerning allostery in live cells.
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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.