ReviewBioscience reports2012
Exploring the dominant role of Cav1 channels in signalling to the nucleus.
Review in Bioscience reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 67 citations in OpenAlex.
- Aberrant calcium signaling and neuronal activity in the L271H CACNA1D (Cav1.3) iPSC model of neurodevelopmental disease.Molecular psychiatry · 2026Article
- From venom peptides to neurotherapeutics: BmK defensins and short-chain peptides as modulators of ion channels.Frontiers in pharmacology · 2026Review
- Cinnarizine, a Calcium Channel Blocker, Partially Prevents the Striatal Dopamine Decline and Loss of Nigral Dopamine Neurons in the Lactacystin-Induced Rat Model of Parkinson's Disease.International journal of molecular sciences · 2025Article
- CaMKII clusters neuronal LTCCs in biomolecular condensates to gate excitation-transcription coupling.bioRxiv : the preprint server for biology · 2025Article
- Role of Cav1.3 Channels in Brain-Heart Interactions: An Unexpected Journey.Biomedicines · 2025Review
- Ion Channels in Odor Information Processing of Neural Circuits of the Vertebrate Olfactory Bulb.International journal of molecular sciences · 2024Review
- The human channel gating-modifying A749G CACNA1D (Cav1.3) variant induces a neurodevelopmental syndrome-like phenotype in mice.JCI insight · 2023Article
- Caldendrin represses neurite regeneration and growth in dorsal root ganglion neurons.Scientific reports · 2023Article
- CACNA1C-Related Channelopathies.Handbook of experimental pharmacology · 2023Review
- Mechanisms and physiological implications of cooperative gating of clustered ion channels.Physiological reviews · 2022Review
- Cytosolic peptides encoding CaCommunications biology · 2022Article
- Regulation of neuronal excitation-transcription coupling by Kv2.1-induced clustering of somatic L-type CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Snapin Specifically Up-Regulates CaInternational journal of molecular sciences · 2021Article
- Roles for α-Synuclein in Gene Expression.Genes · 2021Review
- Design of an Imaging Probe to Monitor Real-Time Redistribution of L-type Voltage-Gated Calcium Channels in Astrocytic Glutamate Signaling.Molecular imaging and biology · 2021Article
- Article
- Voltage-Gated CaFrontiers in synaptic neuroscience · 2021Review
- Functional Consequences of Calcium-Dependent Synapse-to-Nucleus Communication: Focus on Transcription-Dependent Metabolic Plasticity.Cold Spring Harbor perspectives in biology · 2020Review
- High-Voltage-Activated Calcium Channel in the Afferent Pain Pathway: An Important Target of Pain Therapies.Neuroscience bulletin · 2019Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Calcium is important in controlling nuclear gene expression through the activation of multiple signal-transduction pathways in neurons. Compared with other voltage-gated calcium channels, Ca(V)1 channels demonstrate a considerable advantage in signalling to the nucleus. In this review, we summarize the recent progress in elucidating the mechanisms involved. Ca(V)1 channels, already advantaged in their responsiveness to depolarization, trigger communication with the nucleus by attracting colocalized clusters of activated CaMKII (Ca(2+)/calmodulin-dependent protein kinase II). Ca(V)2 channels lack this ability, but must work at a distance of >1 μm from the Ca(V)1-CaMKII co-clusters, which hampers their relative efficiency for a given rise in bulk [Ca(2+)](i) (intracellular [Ca(2+)]). Moreover, Ca(2+) influx from Ca(V)2 channels is preferentially buffered by the ER (endoplasmic reticulum) and mitochondria, further attenuating their effectiveness in signalling to the nucleus.
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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.