Evidence map›Paper›PMID 24462093›Full record

ReviewNeuron2014

CaMKII: claiming center stage in postsynaptic function and organization.

Johannes W Hell

Open access · bronzeAbstract readReview
In one paragraph

Review in Neuron, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 210 papers.

0numbers the graph read from it
0cells of the map it votes in
210citing papers in PubMed
13.5field-weighted citation impact, top 1% 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

210 citing papers in PubMed, 362 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
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  11. Widely Used CaMKII Regulatory Segment Mutations Cause Tight Actinin Binding and Dendritic Spine Enlargement in Unstimulated Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  12. Review
  13. Article
  14. Activity-Dependent Increases in Quantal Size at theJournal of developmental biology · 2025
    Article
  15. Article
  16. An AlphaFold guided model for the evolution of the CaMKII interactome.bioRxiv : the preprint server for biology · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. Review

150 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Johannes W HellDepartment of Pharmacology, University of California, Davis, Davis, CA 95615, USA. Electronic address: jwhell@ucdavis.edu.
University of California, Davis · US

Funding

Subcellular Localization of Cav1.2 by alpha-actininR01AG017502 · NIA · UNIVERSITY OF WISCONSIN MADISON · PI HELL, JOHANNES W · 2000 to 2011
$3.3M
POSTSYNAPTIC SIGNALING PATHWAYSR01NS035563 · NINDS · UNIVERSITY OF WISCONSIN MADISON · PI HELL, JOHANNES W · 1997 to 2010
$3.1M
Signaling by cAMP within postsynaptic nano domains R01NS078792R01NS078792 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HELL, JOHANNES W · 2012 to 2016
$2.0M
NIA NIH HHS R01 AG017502NIA NIH HHS R01AG017502NINDS NIH HHS R01 NS035563NINDS NIH HHS R01NS035563NINDS NIH HHS R01 NS078792NINDS NIH HHS R01NS078792
6 · The paper itself

Abstract

While CaMKII has long been known to be essential for synaptic plasticity and learning, recent work points to new dimensions of CaMKII function in the nervous system, revealing that CaMKII also plays an important role in synaptic organization. Ca(2+)-triggered autophosphorylation of CaMKII not only provides molecular memory by prolonging CaMKII activity during long-term plasticity (LTP) and learning but also represents a mechanism for autoactivation of CaMKII's multifaceted protein-docking functions. New details are also emerging about the distinct roles of CaMKIIα and CaMKIIβ in synaptic homeostasis, further illustrating the multilayered and complex nature of CaMKII's involvement in synaptic regulation. Here, I review novel molecular and functional insight into how CaMKII supports synaptic function.

Indexed as

Models, MolecularAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Nervous SystemNeuronal PlasticitySynapsesCalcium-Calmodulin-Dependent Protein Kinase Type 2

Identifiers

PMID24462093
PMCPMC4570830
OpenAlexW2086121847

What OpenQuestion holds

Textmetadata
LicenceTDM
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.