ArticleMolecular brain2017
A T-type channel-calmodulin complex triggers αCaMKII activation.
Article in Molecular brain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 40 citations in OpenAlex.
- CaMKII modulates memory destabilization by regulating the interaction of theta and gamma oscillations.Frontiers in cellular neuroscience · 2025Article
- The T-type calcium channelosome.Pflugers Archiv : European journal of physiology · 2024Review
- Calmodulin Mutations in Human Disease.Channels (Austin, Tex.) · 2023Review
- Effects of progesterone on T-type-CaNeural regeneration research · 2022Article
- Article
- Case Report: Developmental Delay and Acute Neuropsychiatric Episodes Associated With aFrontiers in pharmacology · 2022Article
- Simultaneous administration of cocaine and caffeine dysregulates HCN and T-type channels.Psychopharmacology · 2021Article
- Neuronal Cav3 channelopathies: recent progress and perspectives.Pflugers Archiv : European journal of physiology · 2020Review
- FMRP(1-297)-tat restores ion channel and synaptic function in a model of Fragile X syndrome.Nature communications · 2020Article
- Genetic T-type calcium channelopathies.Journal of medical genetics · 2020Review
- TAF1-gene editing alters the morphology and function of the cerebellum and cerebral cortex.Neurobiology of disease · 2019Article
- A novel phospho-modulatory mechanism contributes to the calcium-dependent regulation of T-type CaScientific reports · 2019Article
- T-type calcium channels functionally interact with spectrin (α/β) and ankyrin B.Molecular brain · 2018Article
- Activity-Dependent Facilitation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Calmodulin (CaM) is an important signaling molecule that regulates a vast array of cellular functions by activating second messengers involved in cell function and plasticity. Low voltage-activated calcium channels of the Cav3 family have the important role of mediating low threshold calcium influx, but were not believed to interact with CaM. We find a constitutive association between CaM and the Cav3.1 channel at rest that is lost through an activity-dependent and Cav3.1 calcium-dependent CaM dissociation. Moreover, Cav3 calcium influx is sufficient to activate αCaMKII in the cytoplasm in a manner that depends on an intact Cav3.1 C-terminus needed to support the CaM interaction. Our findings thus establish that T-type channel calcium influx invokes a novel dynamic interaction between CaM and Cav3.1 channels to trigger a signaling cascade that leads to αCaMKII activation.
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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.