Evidence map›Paper›PMID 32611770›Full record

ArticleThe Journal of biological chemistry2020

CaMKII enhances voltage-gated sodium channel Nav1.6 activity and neuronal excitability.

Agnes S Zybura, Anthony J Baucum, Anthony M Rush, Theodore R Cummins, Andy Hudmon

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Inhibition of the GSK3β/Nav1.6 complex suppresses early-stage Alzheimer's hyperexcitability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  7. Review
  8. Article
  9. Voltage-Gated NaLife (Basel, Switzerland) · 2023
    Review
  10. T-type CaCell reports · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Role of CaFrontiers in molecular neuroscience · 2022
    Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Agnes S ZyburaProgram in Medical Neuroscience, Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Anthony J BaucumProgram in Medical Neuroscience, Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana, USA.ORCID 0000-0002-4756-9865
Anthony M RushMetrion Biosciences Limited, Cambridge, United Kingdom.
Theodore R CumminsProgram in Medical Neuroscience, Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Andy HudmonProgram in Medical Neuroscience, Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana, USA ahudmon@purdue.edu.
University of Indianapolis · USIndiana University School of MedicinePurdue University West Lafayette · US

Funding

Project 3 - Development and investigation of murine models of channelopathy-associated epilepsyU54NS108874 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GEORGE, ALFRED L. · 2018 to 2022
$12.1M
Sodium channels and electrogenesis in sensory neuronsR01NS053422 · NINDS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI CUMMINS, THEODORE R · 2006 to 2019
$4.6M
Spinophilin function in regulating pathological responses to psychostimulant drugR33DA041876 · NIDA · INDIANA UNIVERSITY INDIANAPOLIS · PI BAUCUM, ANTHONY J. · 2018 to 2020
$1.2M
NIDA NIH HHS R33 DA041876NINDS NIH HHS R01 NS053422NINDS NIH HHS U54 NS108874
6 · The paper itself

Abstract

Nav1.6 is the primary voltage-gated sodium channel isoform expressed in mature axon initial segments and nodes, making it critical for initiation and propagation of neuronal impulses. Thus, Nav1.6 modulation and dysfunction may have profound effects on input-output properties of neurons in normal and pathological conditions. Phosphorylation is a powerful and reversible mechanism regulating ion channel function. Because Nav1.6 and the multifunctional Ca

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell LineCells, CulturedFemaleHEK293 CellsHumansMaleMice, Inbred C57BLNAV1.6 Voltage-Gated Sodium ChannelNeuronal PlasticityNeuronsPatch-Clamp TechniquesPurkinje CellsCalcium-Calmodulin-Dependent Protein Kinase Type 2CAMK2A protein, humanNAV1.6 Voltage-Gated Sodium ChannelSCN8A protein, humanCa2+/calmodulin-dependent protein kinase II (CaMKII)CaMKIIelectrophysiologyNav1.6phosphoproteomicsphosphorylationpost-translational modification (PTM)sodium channel

Identifiers

PMID32611770
PMCPMC7450116
OpenAlexW3039444660

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.