Evidence map›Paper›PMID 29483835›Full record

ArticleInternational journal of biological sciences2018

Loss of p21 promoted tumorigenesis in the background of telomere dysfunctions induced by TRF2 and Wrn deficiency.

Xiaoyu Si, Chihao Shao, Jing Li, Shuting Jia, Wenru Tang, Jihong Zhang, Julun Yang, Xiaoming Wu, Ying Luo

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. The Distinct Function of p21Frontiers in genetics · 2021
    Article
  4. Article
  5. Telomere length and telomerase activity during folliculogenesis in mammals.The Journal of reproduction and development · 2018
    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

9 authors at 3 institutions in 1 country.

Xiaoyu SiLab of Molecular Genetics of Aging & Tumor, Faculty of Medicine, Kunming University of Science & Technology, 727 South Jing Ming Road, Chenggong County, Kunming, Yunnan Province, China, 650500.
Chihao ShaoLab of Molecular Genetics of Aging & Tumor, Faculty of Medicine, Kunming University of Science & Technology, 727 South Jing Ming Road, Chenggong County, Kunming, Yunnan Province, China, 650500.
Jing LiLab of Molecular Genetics of Aging & Tumor, Faculty of Medicine, Kunming University of Science & Technology, 727 South Jing Ming Road, Chenggong County, Kunming, Yunnan Province, China, 650500.
Shuting JiaLab of Molecular Genetics of Aging & Tumor, Faculty of Medicine, Kunming University of Science & Technology, 727 South Jing Ming Road, Chenggong County, Kunming, Yunnan Province, China, 650500.
Wenru TangLab of Molecular Genetics of Aging & Tumor, Faculty of Medicine, Kunming University of Science & Technology, 727 South Jing Ming Road, Chenggong County, Kunming, Yunnan Province, China, 650500.
Jihong ZhangLab of Molecular Genetics of Aging & Tumor, Faculty of Medicine, Kunming University of Science & Technology, 727 South Jing Ming Road, Chenggong County, Kunming, Yunnan Province, China, 650500.
Julun YangFaculty of Environmental Science and Engineering, Kunming University of Science & Technology, 727 South Jing Ming Road, Chenggong County, Kunming, Yunnan Province, China, 650500.
Xiaoming WuLab of Molecular Genetics of Aging & Tumor, Faculty of Medicine, Kunming University of Science & Technology, 727 South Jing Ming Road, Chenggong County, Kunming, Yunnan Province, China, 650500.
Ying LuoLab of Molecular Genetics of Aging & Tumor, Faculty of Medicine, Kunming University of Science & Technology, 727 South Jing Ming Road, Chenggong County, Kunming, Yunnan Province, China, 650500.
Kunming University of Science and Technology · CNQilu University of Technology · CNShandong Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Werner syndrome (WS) is a rare autosomal recessive progeria disease with genetic instability/cancer predisposition, thus a good model in understanding aging related carcinogenesis. Telomere dysfunction induced cellular senescence is essential in the manifestation of the WS phenotype. Our previous data has shown that p21 (encoded by

Indexed as

AnimalsCarcinogenesisCyclin-Dependent Kinase Inhibitor p21Gene Knockdown TechniquesGenetic Predisposition to DiseaseGenomic InstabilityMiceTumor Suppressor Protein p53Werner SyndromeWerner Syndrome HelicaseCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21Tumor Suppressor Protein p53Werner Syndrome HelicaseWrn protein, mousep21senescencetelomere dysfunctiontumorigenesisWrn

Identifiers

PMID29483835
PMCPMC5821038
OpenAlexW2793402904

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.