ArticlePloS one2011
Kv7 channels can function without constitutive calmodulin tethering.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Calmodulation meta-analysis: predicting calmodulin binding via canonical motif clustering.The Journal of general physiology · 2014Pooled it
- Redox regulation of KeLife · 2023Article
- Activation of SGK1.1 Upregulates the M-current in the Presence of Epilepsy Mutations.Frontiers in molecular neuroscience · 2021Article
- Atomistic Insights of Calmodulin Gating of Complete Ion Channels.International journal of molecular sciences · 2020Review
- Calmodulin: A Multitasking Protein in Kv7.2 Potassium Channel Functions.Biomolecules · 2018Review
- Lack of correlation between surface expression and currents in epileptogenic AB-calmodulin binding domain Kv7.2 potassium channel mutants.Channels (Austin, Tex.) · 2018Article
- Calmodulin confers calcium sensitivity to the stability of the distal intracellular assembly domain of Kv7.2 channels.Scientific reports · 2017Article
- Differential Regulation of PI(4,5)PFrontiers in molecular neuroscience · 2017Article
- Voltage-dependent gating of KCNH potassium channels lacking a covalent link between voltage-sensing and pore domains.Nature communications · 2015Article
- Polarized axonal surface expression of neuronal KCNQ potassium channels is regulated by calmodulin interaction with KCNQ2 subunit.PloS one · 2014Article
- Pivoting between calmodulin lobes triggered by calcium in the Kv7.2/calmodulin complex.PloS one · 2014Article
- The neuronal serum- and glucocorticoid-regulated kinase 1.1 reduces neuronal excitability and protects against seizures through upregulation of the M-current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Structure of a Ca(2+)/CaM:Kv7.4 (KCNQ4) B-helix complex provides insight into M current modulation.Journal of molecular biology · 2013Article
- Structural insights into neuronal K+ channel-calmodulin complexes.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Surface expression and subunit specific control of steady protein levels by the Kv7.2 helix A-B linker.PloS one · 2012Article
- Regions of KCNQ K(+) channels controlling functional expression.Frontiers in physiology · 2012Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
M-channels are voltage-gated potassium channels composed of Kv7.2-7.5 subunits that serve as important regulators of neuronal excitability. Calmodulin binding is required for Kv7 channel function and mutations in Kv7.2 that disrupt calmodulin binding cause Benign Familial Neonatal Convulsions (BFNC), a dominantly inherited human epilepsy. On the basis that Kv7.2 mutants deficient in calmodulin binding are not functional, calmodulin has been defined as an auxiliary subunit of Kv7 channels. However, we have identified a presumably phosphomimetic mutation S511D that permits calmodulin-independent function. Thus, our data reveal that constitutive tethering of calmodulin is not required for Kv7 channel function.
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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.