Evidence map›Paper›PMID 40282367›Full record

ReviewGenes2025

The Molecular Intersection of NEK1, C21ORF2, Cyclin F, and VCP in ALS Pathogenesis.

Yasuaki Watanabe, Tadashi Nakagawa, Makiko Nakagawa, Keiko Nakayama

Abstract readReview
In one paragraph

Review in Genes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Frontiers in aging neuroscience · 2026
    Article
  6. Review
  7. 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

4 authors.

Yasuaki WatanabeDepartment of Neurology, Graduate School of Medicine, Tohoku University, Sendai 980-8575, Japan.ORCID 0009-0006-3347-1628
Tadashi NakagawaDivision of Cell Proliferation, United Centers for Advanced Research and Translational Medicine, Graduate School of Medicine, Tohoku University, Sendai 980-8575, Japan.ORCID 0000-0001-8872-6129
Makiko NakagawaInstitute of Gene Research, Yamaguchi University Science Research Center, Ube 755-8505, Japan.
Keiko NakayamaDivision of Cell Proliferation, United Centers for Advanced Research and Translational Medicine, Graduate School of Medicine, Tohoku University, Sendai 980-8575, Japan.ORCID 0000-0003-0134-6401

Funding

Japan Society for the Promotion of Science 23K06367
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder characterized by the progressive degeneration of motor neurons, leading to muscle weakness, paralysis, and death. Although significant progress has been made in understanding ALS, its molecular mechanisms remain complex and multifactorial. This review explores the potential convergent mechanisms underlying ALS pathogenesis, focusing on the roles of key proteins including NEK1, C21ORF2, cyclin F, VCP, and TDP-43. Recent studies suggest that mutations in

Indexed as

Amyotrophic Lateral SclerosisCyclinsNIMA-Related Kinase 1Valosin Containing ProteinAnimalsDNA-Binding ProteinsDNA DamageDNA RepairHumansMutationCCNF protein, humanCyclinsDNA-Binding ProteinsNEK1 protein, humanNIMA-Related Kinase 1TARDBP protein, humanValosin Containing ProteinVCP protein, humanamyotrophic lateral sclerosis (ALS)C21ORF2cyclin FDNA damage repairNEK1neurodegenerationprotein homeostasisTDP-43 aggregationVCP

Identifiers

PMID40282367
PMCPMC12026591

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.