Evidence map›Paper›PMID 36114168›Full record

ArticleNature communications2022

WRN promotes bone development and growth by unwinding SHOX-G-quadruplexes via its helicase activity in Werner Syndrome.

Yuyao Tian, Wuming Wang, Sofie Lautrup, Hui Zhao, Xiang Li, Patrick Wai Nok Law, Ngoc-Duy Dinh, Evandro Fei Fang, Hoi Hung Cheung, Wai-Yee Chan

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Establishment and application of a zebrafish model of Werner syndrome identifies sapanisertib as a potential antiaging drug.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. "Bone-SASP" in Skeletal Aging.Calcified tissue international · 2023
    Review
  13. Review
  14. Article
  15. 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

10 authors at 3 institutions in 3 countries.

Yuyao TianSchool of Biomedical Sciences, Faculty of Medicine, the Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR.
Wuming WangSchool of Biomedical Sciences, Faculty of Medicine, the Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR.
Sofie LautrupDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1478, Lørenskog, Norway.ORCID http://orcid.org/0000-0002-6632-7853
Hui ZhaoSchool of Biomedical Sciences, Faculty of Medicine, the Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR.ORCID http://orcid.org/0000-0001-8160-6415
Xiang LiCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Patrick Wai Nok LawSchool of Biomedical Sciences, Faculty of Medicine, the Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR.
Ngoc-Duy DinhDepartment of Biomedical Engineering, the Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR.ORCID http://orcid.org/0000-0002-4964-7038
Evandro Fei FangDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1478, Lørenskog, Norway.
Hoi Hung CheungSchool of Biomedical Sciences, Faculty of Medicine, the Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR.
Wai-Yee ChanSchool of Biomedical Sciences, Faculty of Medicine, the Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR. chanwy@cuhk.edu.hk.ORCID http://orcid.org/0000-0002-9714-0936
Chinese University of Hong Kong · HKUniversity of Oslo · NOShanghai Institute of Nutrition and Health · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Werner Syndrome (WS) is an autosomal recessive disorder characterized by premature aging due to mutations of the WRN gene. A classical sign in WS patients is short stature, but the underlying mechanisms are not well understood. Here we report that WRN is indispensable for chondrogenesis, which is the engine driving the elongation of bones and determines height. Zebrafish lacking wrn exhibit impairment of bone growth and have shorter body stature. We pinpoint the function of WRN to its helicase domain. We identify short-stature homeobox (SHOX) as a crucial and direct target of WRN and find that the WRN helicase core regulates the transcriptional expression of SHOX via unwinding G-quadruplexes. Consistent with this, shox

Indexed as

G-QuadruplexesWerner SyndromeAnimalsBone DevelopmentDNA-Binding ProteinsGenes, HomeoboxRecQ HelicasesWerner Syndrome HelicaseZebrafishDNA-Binding ProteinsRecQ HelicasesWerner Syndrome Helicase

Identifiers

PMID36114168
PMCPMC9481537
OpenAlexW4295996519

What OpenQuestion holds

Textmetadata
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.