Evidence map›Paper›PMID 25863357›Full record

ArticleBiological psychiatry2015

Inhibition of 14-3-3 Proteins Leads to Schizophrenia-Related Behavioral Phenotypes and Synaptic Defects in Mice.

Molly Foote, Haifa Qiao, Kourtney Graham, Yuying Wu, Yi Zhou

Abstract read
In one paragraph

Article in Biological psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

45 citing papers in PubMed, 62 citations in OpenAlex.

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  17. The 14-3-3 Protein Family and Schizophrenia.Frontiers in molecular neuroscience · 2022
    Review
  18. Article
  19. Cofilin Signaling in the CNS Physiology and Neurodegeneration.International journal of molecular sciences · 2021
    Review
  20. Review
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 1 institution in 1 country.

Molly FooteDepartment of Biomedical Sciences, Florida State University, College of Medicine, Tallahassee, Florida.
Haifa QiaoDepartment of Biomedical Sciences, Florida State University, College of Medicine, Tallahassee, Florida.
Kourtney GrahamDepartment of Biomedical Sciences, Florida State University, College of Medicine, Tallahassee, Florida.
Yuying WuDepartment of Biomedical Sciences, Florida State University, College of Medicine, Tallahassee, Florida.
Yi ZhouDepartment of Biomedical Sciences, Florida State University, College of Medicine, Tallahassee, Florida.. Electronic address: yzhou@fsu.edu.
Florida State University · US

Funding

Functions of the N-type Ca Channel/14-3-3 InteractionR01NS050355 · NINDS · FLORIDA STATE UNIVERSITY · PI ZHOU, YI · 2007 to 2011
$1.4M
NINDS NIH HHS NS50355NINDS NIH HHS R01 NS050355
6 · The paper itself

Abstract

backgroundThe 14-3-3 family of proteins is implicated in the regulation of several key neuronal processes. Previous human and animal studies suggested an association between 14-3-3 dysregulation and schizophrenia.

methodsWe characterized behavioral and functional changes in transgenic mice that express an isoform-independent 14-3-3 inhibitor peptide in the brain.

resultsWe recently showed that 14-3-3 functional knockout mice (FKO) exhibit impairments in associative learning and memory. We report here that these 14-3-3 FKO mice display other behavioral deficits that correspond to the core symptoms of schizophrenia. These behavioral deficits may be attributed to alterations in multiple neurotransmission systems in the 14-3-3 FKO mice. In particular, inhibition of 14-3-3 proteins results in a reduction of dendritic complexity and spine density in forebrain excitatory neurons, which may underlie the altered synaptic connectivity in the prefrontal cortical synapse of the 14-3-3 FKO mice. At the molecular level, this dendritic spine defect may stem from dysregulated actin dynamics secondary to a disruption of the 14-3-3-dependent regulation of phosphorylated cofilin.

conclusionsCollectively, our data provide a link between 14-3-3 dysfunction, synaptic alterations, and schizophrenia-associated behavioral deficits.

Indexed as

Schizophrenic PsychologySynaptic Transmission14-3-3 ProteinsAnimalsAntipsychotic AgentsBehavior, AnimalCateninsCerebral CortexClozapineCofilin 1Delta CateninDendritesDisease Models, AnimalDopamineHaloperidolMice14-3-3 ProteinsAntipsychotic AgentsCateninsClozapineCofilin 1Delta CatenindifopeinDopamineHaloperidolProteinsReceptors, Dopamine14-3-3 ProteinsDendritic spinesNeurotransmissionPrefrontal cortexSchizophreniaTransgenic mouse model

Identifiers

PMID25863357
PMCPMC4544659
OpenAlexW2079724117

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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.