ReviewChannels (Austin, Tex.)2016
Decalmodulation of Cav1 channels by CaBPs.
Review in Channels (Austin, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 22 citations in OpenAlex.
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- Comprehensive Characterization of a Subfamily of CaeNeuro · 2024Article
- Chemical shift assignments of the C-terminal domain of CaBP1 bound to the IQ-motif of voltage-gated CaBiomolecular NMR assignments · 2022Article
- Calcium Channels in Retinal Function and Disease.Annual review of vision science · 2022Review
- L-Type CaBiomolecules · 2021Review
- NeuriteNet: A convolutional neural network for assessing morphological parameters of neurite growth.Journal of neuroscience methods · 2021Article
- Encoding sound in the cochlea: from receptor potential to afferent discharge.The Journal of physiology · 2021Review
- Voltage-Gated CaFrontiers in synaptic neuroscience · 2021Review
- RBP2 stabilizes slow Cav1.3 CaPflugers Archiv : European journal of physiology · 2020Article
- 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
- CaNeuroscience · 2018Article
- CaBP1 regulates CaMolecular and cellular neurosciences · 2018Article
- Biophysical and functional characterization of hippocalcin mutants responsible for human dystonia.Human molecular genetics · 2017Article
- Characterization of C-terminal Splice Variants of Cav1.4 Ca2+ Channels in Human Retina.The Journal of biological chemistry · 2016Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ca(2+)-dependent inactivation (CDI) is a negative feedback regulation of voltage-gated Cav1 and Cav2 channels that is mediated by the Ca(2+) sensing protein, calmodulin (CaM), binding to the pore-forming Cav α1 subunit. David Yue and his colleagues made seminal contributions to our understanding of this process, as well as factors that regulate CDI. Important in this regard are members of a family of Ca(2+) binding proteins (CaBPs) that are related to calmodulin. CaBPs are expressed mainly in neural tissues and can antagonize CaM-dependent CDI for Cav1 L-type channels. This review will focus on the roles of CaBPs as Cav1-interacting proteins, and the significance of these interactions for vision, hearing, and neuronal Ca(2+) signaling events.
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What OpenQuestion holds
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.