Evidence map›Paper›PMID 37550059›Full record

ArticleeNeuro2023

A Novel Interaction between MFN2/Marf and MARK4/PAR-1 Is Implicated in Synaptic Defects and Mitochondrial Dysfunction.

Yeongmi Cheon, Sunggyu Yoon, Jae-Hyuk Lee, Kiyoung Kim, Hyung-Jun Kim, Sung Wook Hong, Ye-Rang Yun, Jiwon Shim, Sung-Hak Kim, Bingwei Lu and 2 more

Open access · goldAbstract read
In one paragraph

Article in eNeuro, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. From Stress to Synapse: The Neuronal Atrophy Pathway to Mood Dysregulation.International journal of molecular sciences · 2025
    Review
  2. Article
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

12 authors at 7 institutions in 3 countries.

Yeongmi CheonGwangju Center, Korea Basic Science Institute, Gwangju 61751, Korea.ORCID 0000-0001-8986-9308
Sunggyu YoonGwangju Center, Korea Basic Science Institute, Gwangju 61751, Korea.
Jae-Hyuk LeeGwangju Center, Korea Basic Science Institute, Gwangju 61751, Korea.ORCID 0000-0002-9782-4297
Kiyoung KimDepartment of Medical Science, Soonchunhyang University, Asan 31538, Korea.
Hyung-Jun KimDementia Research Group, Korea Brain Research Institute, Daegu 41068, Korea.
Sung Wook HongKimchi Functionality Research Group, World Institute of Kimchi, Gwangju 61755, Korea.
Ye-Rang YunKimchi Functionality Research Group, World Institute of Kimchi, Gwangju 61755, Korea.
Jiwon ShimDepartment of Life Science, College of Natural Science, Hanyang University, Seoul 04763, Korea.
Sung-Hak KimLaboratory of Molecular Biochemistry, Chonnam National University, Gwangju 61186, Korea.
Bingwei LuDepartment of Pathology, Stanford University School of Medicine, Stanford, California 94305 soolee@kbsi.re.kr bingwei@stanford.edu mihyelee@sch.ac.kr.
Mihye LeeSoonchunhyang Institute of Medi-Bio Science, Soonchunhyang University, Cheonan 31151, Korea soolee@kbsi.re.kr bingwei@stanford.edu mihyelee@sch.ac.kr.
Seongsoo LeeGwangju Center, Korea Basic Science Institute, Gwangju 61751, Korea soolee@kbsi.re.kr bingwei@stanford.edu mihyelee@sch.ac.kr.
Korea Basic Science Institute · KRChonnam National University · KRGwangju Institute of Science and Technology · KRSoonchunhyang University · KRHanyang University · KRKorea Brain Research Institute · KRStanford University · US

Funding

Role of PAR-1 Kinase in SynaptogenesisR01MH080378 · NIMH · STANFORD UNIVERSITY · PI LU, BINGWEI · 2009 to 2018
$4.0M
NIMH NIH HHS R01 MH080378
6 · The paper itself

Abstract

As cellular energy powerhouses, mitochondria undergo constant fission and fusion to maintain functional homeostasis. The conserved dynamin-like GTPase, Mitofusin2 (MFN2)/mitochondrial assembly regulatory factor (Marf), plays a role in mitochondrial fusion, mutations of which are implicated in age-related human diseases, including several neurodegenerative disorders. However, the regulation of MFN2/Marf-mediated mitochondrial fusion, as well as the pathologic mechanism of neurodegeneration, is not clearly understood. Here, we identified a novel interaction between MFN2/Marf and microtubule affinity-regulating kinase 4 (MARK4)/PAR-1. In the

Indexed as

Drosophila ProteinsMitochondriaSynapsesAnimalsDrosophilaGlycogen Synthase Kinase 3GTP PhosphohydrolasesHumansMammalsMembrane ProteinsMicrotubulesMitochondrial ProteinsProtein Serine-Threonine KinasesDrosophila ProteinsGlycogen Synthase Kinase 3GTP PhosphohydrolasesMarf protein, DrosophilaMARK4 protein, humanMembrane ProteinsMFN2 protein, humanMitochondrial ProteinsPar-1 protein, DrosophilaProtein Serine-Threonine KinasesDrosophila melanogasterMARK4/PAR-1MFN2/Marfmitochondrial dynamicsneurodegenerative disease

Identifiers

PMID37550059
PMCPMC10444538
OpenAlexW4385622411

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.