Evidence map›Paper›PMID 31712410›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Mutant p53 antagonizes p63/p73-mediated tumor suppression via Notch1.

Jin Zhang, Wenqiang Sun, Xiangmudong Kong, Yanhong Zhang, Hee Jung Yang, Cong Ren, Yuqian Jiang, Mingyi Chen, Xinbin Chen

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

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Reactivation ofInternational journal of molecular sciences · 2026
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  13. p73α1, a p73 C-terminal isoform, regulates tumor suppression and the inflammatory response via Notch1.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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 2 institutions in 1 country.

Jin ZhangComparative Oncology Laboratory, Schools of Veterinary Medicine and Medicine, University of California, Davis, CA 95616; jinzhang@ucdavis.edu xbchen@ucdavis.edu.
Wenqiang SunComparative Oncology Laboratory, Schools of Veterinary Medicine and Medicine, University of California, Davis, CA 95616.
Xiangmudong KongComparative Oncology Laboratory, Schools of Veterinary Medicine and Medicine, University of California, Davis, CA 95616.
Yanhong ZhangComparative Oncology Laboratory, Schools of Veterinary Medicine and Medicine, University of California, Davis, CA 95616.
Hee Jung YangComparative Oncology Laboratory, Schools of Veterinary Medicine and Medicine, University of California, Davis, CA 95616.
Cong RenComparative Oncology Laboratory, Schools of Veterinary Medicine and Medicine, University of California, Davis, CA 95616.
Yuqian JiangComparative Oncology Laboratory, Schools of Veterinary Medicine and Medicine, University of California, Davis, CA 95616.
Mingyi ChenDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390.ORCID 0000-0001-6754-0480
Xinbin ChenComparative Oncology Laboratory, Schools of Veterinary Medicine and Medicine, University of California, Davis, CA 95616; jinzhang@ucdavis.edu xbchen@ucdavis.edu.
University of California, Davis · USThe University of Texas Southwestern Medical Center · US

Funding

MECHANISM OF P73 DEPENDENT TUMOR SUPPRESSIONR01CA081237 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 1999 to 2022
$6.8M
The feedback loop between ferredoxin reductase and the p53 family in tumor suppressionR01CA224433 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2018 to 2022
$2.0M
The role of the p63-RBM38 loop in tumor suppressionR01CA195828 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA081237NCI NIH HHS R01 CA195828NCI NIH HHS R01 CA224433
6 · The paper itself

Abstract

p53 is the most frequently mutated gene in human cancers and mutant p53 has a gain of function (GOF) that promotes tumor progression and therapeutic resistance. One of the major GOF activities of mutant p53 is to suppress 2 other p53 family proteins, p63 and p73. However, the molecular basis is not fully understood. Here, we examined whether mutant p53 antagonizes p63/p73-mediated tumor suppression in vivo by using mutant p53-R270H knockin and

Indexed as

AnimalsCell Line, TumorExtracellular Matrix ProteinsGene Expression Regulation, NeoplasticHumansMice, Mutant StrainsMutationPrecursor T-Cell Lymphoblastic Leukemia-LymphomaPromoter Regions, GeneticReceptor, Notch1Trans-ActivatorsTranscription Factor HES-1Tumor Protein p73Tumor Suppressor Protein p53Ecm1 protein, mouseExtracellular Matrix ProteinsHes1 protein, mouseNotch1 protein, mouseReceptor, Notch1Trans-ActivatorsTranscription Factor HES-1Trp53 protein, mouseTrp63 protein, mouseTrp73 protein, mouseTumor Protein p73Tumor Suppressor Protein p53GOFmutant p53Notch1p63/p73T-ALL

Identifiers

PMID31712410
PMCPMC6883818
OpenAlexW2988238922

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.