Evidence map›Paper›PMID 42311417›Full record

ReviewFrontiers in molecular neuroscience2026

Calcium signaling and postsynaptic density dynamics: the roles of calmodulin in synaptic protein regulation.

Keyaa Dilip Shah, Yonghong Zhang

Abstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Keyaa Dilip ShahSchool of Integrative Biological and Chemical Sciences (SIBCS), University of Texas Rio Grande Valley, Edinburg, TX, United States.
Yonghong ZhangSchool of Integrative Biological and Chemical Sciences (SIBCS), University of Texas Rio Grande Valley, Edinburg, TX, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium signaling in neuronal cells is the principal mechanism underlying learning and synaptic plasticity, whereas the postsynaptic density (PSD) is an important center where calcium-dependent processes are organized and regulated. This review explores the roles of calmodulin (CaM) in facilitating calcium-dependent modulation of the activities of synaptic proteins in the PSD. We focus on the molecular processes through which CaM interacts with calcium signals to regulate the function, localization, and interactions of central synaptic proteins, including calcium/calmodulin-dependent protein kinase II (CaMKII), membrane-associated guanylate kinases (MAGUKs), and N-methyl-D-aspartate (NMDA) receptors. We aim to summarize recent advances in structural, biochemical, and imaging studies of how CaM's structural flexibility, calcium binding kinetics, and protein-protein interactions uncover complex regulatory loops that allow exquisite temporal and spatial control over synaptic efficacy. Additionally, research progress on how disruptions of CaM-mediated signaling pathways are linked to neurological diseases, which may be conducive to new potential therapeutic interventions, is discussed.

Indexed as

calciumcalmodulinpostsynaptic densitysynaptic proteinssynaptic regulation

Identifiers

PMID42311417
PMCPMC13269105

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Registered trials

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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.