Evidence map›Paper›PMID 27023172›Full record

ArticleTranslational psychiatry2016

Deletion of JMJD2B in neurons leads to defective spine maturation, hyperactive behavior and memory deficits in mouse.

K Fujiwara, Y Fujita, A Kasai, Y Onaka, H Hashimoto, H Okada, T Yamashita

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.3field-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

25 citing papers in PubMed, 34 citations in OpenAlex.

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  6. Epigenetic effects of herbal medicine.Clinical epigenetics · 2023
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  9. KDM4 Demethylases: Structure, Function, and Inhibitors.Advances in experimental medicine and biology · 2023
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  17. Article
  18. Targeted Downregulation ofJournal of Korean medical science · 2019
    Article
  19. Review
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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

7 authors at 2 institutions in 1 country.

K FujiwaraDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Japan.
Y FujitaDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Japan.
A KasaiLaboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Japan.
Y OnakaLaboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Japan.
H HashimotoLaboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Japan.
H OkadaDepartment of Biochemistry, Kinki University Faculty of Medicine, Sayama, Japan.
T YamashitaDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Japan.
Osaka University · JPKindai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

JMJD2B is a histone demethylase enzyme that regulates gene expression through demethylation of H3K9me3. Although mutations of JMJD2B have been suggested to be responsible for neurodevelopmental disorders, the function of JMJD2B in the central nervous system (CNS) remains to be elucidated. Here we show that JMJD2B has a critical role in the development of the CNS. We observed JMJD2B expression, which was especially strong in the hippocampus, throughout the CNS from embryonic periods through adulthood. We generated neuron-specific JMJD2B-deficient mice using the cre-loxP system. We found an increase in total spine number, but a decrease in mature spines, in the CA1 region of the hippocampus. JMJD2B-deficient mice exhibited hyperactive behavior, sustained hyperactivity in a novel environment, deficits in working memory and spontaneous epileptic-like seizures. Together these observations indicate that JMJD2B mutant mice display symptoms reminiscent of neurodevelopmental disorders. Our findings provide evidence for the involvement of histone demethylation in the formation of functional neural networks during development.

Indexed as

Behavior, AnimalMemory, Short-TermAnimalsCA1 Region, HippocampalDendritic SpinesHyperkinesisJumonji Domain-Containing Histone DemethylasesMemoryMemory DisordersMiceMice, KnockoutNeurodevelopmental DisordersNeuronsSeizuresJumonji Domain-Containing Histone DemethylasesKdm4b protein, mouse

Identifiers

PMID27023172
PMCPMC4872455
OpenAlexW2330332539

What OpenQuestion holds

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LicenceCC BY
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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.