Evidence map›Paper›PMID 37578019›Full record

ArticleEMBO molecular medicine2023

Involvement of casein kinase 1 epsilon/delta (Csnk1e/d) in the pathogenesis of familial Parkinson's disease caused by CHCHD2.

Satoru Torii, Satoko Arakawa, Shigeto Sato, Kei-Ichi Ishikawa, Daisuke Taniguchi, Hajime Tajima Sakurai, Shinya Honda, Yuuichi Hiraoka, Masaya Ono, Wado Akamatsu and 2 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. The Role of Immune Dysfunction in Parkinson's Disease Development.International journal of molecular sciences · 2023
    Review
  9. 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 3 institutions in 2 countries.

Satoru ToriiDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.ORCID 0000-0003-4841-7131
Satoko ArakawaDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.ORCID 0000-0002-4375-1643
Shigeto SatoDepartment of Neurology, School of Medicine, Juntendo University, Tokyo, Japan.
Kei-Ichi IshikawaDepartment of Neurology, School of Medicine, Juntendo University, Tokyo, Japan.ORCID 0000-0003-2305-301X
Daisuke TaniguchiDepartment of Neurology, School of Medicine, Juntendo University, Tokyo, Japan.
Hajime Tajima SakuraiDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Shinya HondaDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Yuuichi HiraokaLaboratory of Molecular Neuroscience, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Masaya OnoDepartment of Clinical Proteomics, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0009-0005-9717-5564
Wado AkamatsuCenter for Genomic and Regenerative Medicine, School of Medicine, Juntendo University, Tokyo, Japan.
Nobutaka HattoriDepartment of Neurology, School of Medicine, Juntendo University, Tokyo, Japan.ORCID 0000-0002-2034-2556
Shigeomi ShimizuDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.ORCID 0000-0002-8437-0791
Tokyo Medical and Dental University · JPJuntendo University · JPNational Cancer Research Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a common neurodegenerative disorder that results from the loss of dopaminergic neurons. Mutations in coiled-coil-helix-coiled-coil-helix domain containing 2 (CHCHD2) gene cause a familial form of PD with α-Synuclein aggregation, and we here identified the pathogenesis of the T61I mutation, the most common disease-causing mutation of CHCHD2. In Neuro2a cells, CHCHD2 is in mitochondria, whereas the T61I mutant (CHCHD2

Indexed as

Casein Kinase 1 epsilonParkinson Diseasealpha-SynucleinAnimalsDNA-Binding ProteinsMiceMutationTranscription Factorsalpha-SynucleinCasein Kinase 1 epsilonDNA-Binding ProteinsTranscription FactorsCHCHD2Csnk1e/dα-Synuclein

Identifiers

PMID37578019
PMCPMC10493588
OpenAlexW4385799051

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.