Evidence map›Paper›PMID 31152587›Full record

ArticleJournal of molecular cell biology2019

ATP11B deficiency leads to impairment of hippocampal synaptic plasticity.

Jiao Wang, Weihao Li, Fangfang Zhou, Ruili Feng, Fushuai Wang, Shibo Zhang, Jie Li, Qian Li, Yajiang Wang, Jiang Xie and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Jiao WangLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Weihao LiLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Fangfang ZhouLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Ruili FengLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Fushuai WangLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Shibo ZhangLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Jie LiLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Qian LiLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Yajiang WangLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Jiang XieSchool of Computer Engineering and Science, Shanghai University, Shanghai, China.
Tieqiao WenLaboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai, China.
Shanghai University · CNShanghai University of Engineering Science · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synaptic plasticity is known to regulate and support signal transduction between neurons, while synaptic dysfunction contributes to multiple neurological and other brain disorders; however, the specific mechanism underlying this process remains unclear. In the present study, abnormal neural and dendritic morphology was observed in the hippocampus following knockout of Atp11b both in vitro and in vivo. Moreover, ATP11B modified synaptic ultrastructure and promoted spine remodeling via the asymmetrical distribution of phosphatidylserine and enhancement of glutamate release, glutamate receptor expression, and intracellular Ca2+ concentration. Furthermore, experimental results also indicate that ATP11B regulated synaptic plasticity in hippocampal neurons through the MAPK14 signaling pathway. In conclusion, our data shed light on the possible mechanisms underlying the regulation of synaptic plasticity and lay the foundation for the exploration of proteins involved in signal transduction during this process.

Indexed as

Adenosine TriphosphatasesAnimalsCalciumCells, CulturedFemaleGlutamic AcidHippocampusMaleMiceMice, KnockoutNeuronal PlasticityNeuronsReceptors, GlutamateSignal TransductionAdenosine TriphosphatasesCalciumGlutamic AcidReceptors, GlutamateATP11Bglutamate receptorsMAPK14 signaling pathwaysynaptic plasticity

Identifiers

PMID31152587
PMCPMC7261485
OpenAlexW2947007462

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.