Evidence map›Paper›PMID 36835200›Full record

ArticleInternational journal of molecular sciences2023

Gain-of-Function p53N236S Mutation Drives the Bypassing of HRas

Hao Yang, Ke Zhang, Yusheng Guo, Xin Guo, Kailong Hou, Jing Hou, Ying Luo, Jing Liu, Shuting Jia

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

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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 1 institution in 1 country.

Hao YangLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Ke ZhangLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Yusheng GuoLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.ORCID 0000-0002-1939-0905
Xin GuoLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Kailong HouLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Jing HouLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Ying LuoLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Jing LiuLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Shuting JiaLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.ORCID 0000-0003-0452-260X
Kunming University of Science and Technology · CN

Funding

National Natural Science Foundation of China 81760262Yunnan "Xing Dian Ren Cai" project YNWR-QNBJ-2019-240
6 · The paper itself

Abstract

One of the key steps in tumorigenic transformation is immortalization in which cells bypass cancer-initiating barriers such as senescence. Senescence can be triggered by either telomere erosion or oncogenic stress (oncogene-induced senescence, OIS) and undergo p53- or Rb-dependent cell cycle arrest. The tumor suppressor p53 is mutated in 50% of human cancers. In this study, we generated p53N236S (p53S) mutant knock-in mice and observed that p53S heterozygous mouse embryonic fibroblasts (

Indexed as

Cellular SenescenceGain of Function MutationTumor Suppressor Protein p53AnimalsFibroblastsMiceMutationProto-Oncogene Proteins p21(ras)Reactive Oxygen SpeciesTranscription Factorsperoxisome-proliferator-activated receptor-gamma coactivator-1Proto-Oncogene Proteins p21(ras)Reactive Oxygen SpeciesTranscription FactorsTumor Suppressor Protein p53oncogene-induced senescencep53 mutantPGC–1α

Identifiers

PMID36835200
PMCPMC9960896
OpenAlexW4320730650

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.