Evidence map›Paper›PMID 37897534›Full record

ArticleCellular and molecular life sciences : CMLS2023

Loss of fragile WWOX gene leads to senescence escape and genome instability.

Hui-Ching Cheng, Po-Hsien Huang, Feng-Jie Lai, Ming-Shiou Jan, Yi-Lin Chen, Szu-Ying Chen, Wan-Li Chen, Chao-Kai Hsu, Wenya Huang, Li-Jin Hsu

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2023. 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
1.6field-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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Zfra Overrides WWOX in Suppressing the Progression of Neurodegeneration.International journal of molecular sciences · 2024
    Review
  4. Frontiers in pediatrics · 2024
    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

10 authors at 4 institutions in 1 country.

Hui-Ching ChengInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Po-Hsien Huang *Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Feng-Jie Lai *Department of Dermatology, Chi Mei Medical Center, Tainan, 71004, Taiwan. lai.fengjie@gmail.com.
Ming-Shiou Jan *Institute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, 40201, Taiwan.
Yi-Lin ChenDepartment of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Szu-Ying ChenDepartment of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Wan-Li ChenMolecular Diagnosis Laboratory, Department of Pathology, National Cheng Kung University Hospital, Tainan, 704302, Taiwan.
Chao-Kai HsuDepartment of Dermatology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Wenya HuangDepartment of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Li-Jin HsuInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan. ljhsu@mail.ncku.edu.tw.ORCID http://orcid.org/0009-0007-9395-6077
National Cheng Kung University · TWNational Cheng Kung University Hospital · TWChi Mei Medical Center · TWChung Shan Medical University · TW

Funding

National Science and Technology Council 103-2320-B-006-002National Science and Technology Council 104-2320-B-006-002National Science and Technology Council 104-2320-B-006-016-MY3National Science and Technology Council 105-2320-B-006-047National Science and Technology Council 106-2320-B-006-018National Science and Technology Council 107-2320-B-006-006National Science and Technology Council 107-2320-B-006-030-MY3National Science and Technology Council 108-2320-B-006-021National Science and Technology Council 109-2320-B-006-059National Science and Technology Council 109-2327-B-006-009National Science and Technology Council 110-2320-B-006-032National Science and Technology Council 110-2320-B-006-062National Science and Technology Council 110-2327-B-006-004
6 · The paper itself

Abstract

Induction of DNA damage response (DDR) to ensure accurate duplication of genetic information is crucial for maintaining genome integrity during DNA replication. Cellular senescence is a DDR mechanism that prevents the proliferation of cells with damaged DNA to avoid mitotic anomalies and inheritance of the damage over cell generations. Human WWOX gene resides within a common fragile site FRA16D that is preferentially prone to form breaks on metaphase chromosome upon replication stress. We report here that primary Wwox knockout (Wwox

Indexed as

Tumor Suppressor Protein p53Ultraviolet RaysAnimalsCellular SenescenceDNAFibroblastsGenomic InstabilityHEK293 CellsHumansMiceTumor Suppressor ProteinsWW Domain-Containing OxidoreductaseDNATumor Suppressor Protein p53Tumor Suppressor ProteinsWW Domain-Containing OxidoreductaseWWOX protein, humanWwox protein, mouseCDK inhibitorsMononucleotide repeat markersPromoter hypermethylationRedox homeostasisReplicative arrestTumor suppressor

Identifiers

PMID37897534
PMCPMC10613160
OpenAlexW4388034513

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.