Evidence map›Paper›PMID 34183057›Full record

ArticleMolecular brain2021

Autophagy activity contributes to the impairment of social recognition in Epac2

Ji-Hye Kwak, You-Kyung Lee, Mi-Hee Jun, Mootaek Roh, Hyunhyo Seo, Juhyun Lee, Kyungmin Lee, Jin-A Lee

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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  3. Article
  4. 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

8 authors at 2 institutions in 1 country.

Ji-Hye Kwak *Behavioral Neural Circuitry and Physiology Laboratory, Department of Anatomy, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, 41944, South Korea.
You-Kyung Lee *Department of Biological Sciences and Biotechnology, College of Life Sciences and Nanotechnology, Hannam University, Daejeon, South Korea.
Mi-Hee Jun *Department of Biological Sciences and Biotechnology, College of Life Sciences and Nanotechnology, Hannam University, Daejeon, South Korea.
Mootaek Roh *Behavioral Neural Circuitry and Physiology Laboratory, Department of Anatomy, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, 41944, South Korea.
Hyunhyo SeoBehavioral Neural Circuitry and Physiology Laboratory, Department of Anatomy, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, 41944, South Korea.
Juhyun LeeBehavioral Neural Circuitry and Physiology Laboratory, Department of Anatomy, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, 41944, South Korea.
Kyungmin LeeBehavioral Neural Circuitry and Physiology Laboratory, Department of Anatomy, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, 41944, South Korea. irislkm@knu.ac.kr.
Jin-A LeeDepartment of Biological Sciences and Biotechnology, College of Life Sciences and Nanotechnology, Hannam University, Daejeon, South Korea. jlmaranatha@gmail.com.ORCID 0000-0002-6757-8371
Hannam University · KRKyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a lysosomal degradation pathway that regulates cellular homeostasis. It is constitutively active in neurons and controls the essential steps of neuronal development, leading to its dysfunction in neurodevelopmental disorders. Although mTOR-associated impaired autophagy has previously been reported in neurodevelopmental disorders, there is lack of information about the dysregulation of mTOR-independent autophagy in neurodevelopmental disorders. In this study, we investigated whether the loss of Epac2, involved in the mTOR-independent pathway, affects autophagy activity and whether the activity of autophagy is associated with social-behavioral phenotypes in mice with Epac2 deficiencies. We observed an accumulation of autophagosomes and a significant increase in autophagic flux in Epac2-deficient neurons, which had no effect on mTOR activity. Next, we examined whether an increase in autophagic activity contributed to the social behavior exhibited in Epac2

Indexed as

AutophagyBehavior, AnimalSocial BehaviorAnimalsGuanine Nucleotide Exchange FactorsMiceSignal TransductionTOR Serine-Threonine KinasesGuanine Nucleotide Exchange FactorsRapgef4 protein, mouseTOR Serine-Threonine KinasesAutophagyEpac2Neurodevelopmental disordersSocial recognition

Identifiers

PMID34183057
PMCPMC8240198
OpenAlexW3175681711

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.