Evidence map›Paper›PMID 35617425›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

p73α1, a p73 C-terminal isoform, regulates tumor suppression and the inflammatory response via Notch1.

Kyra Nicole Laubach, Wensheng Yan, Xiangmudong Kong, Wenqiang Sun, Mingyi Chen, Jin Zhang, Xinbin Chen

Open access · greenAbstract 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, 2022. 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 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. The Role of the Notch1 Signaling Pathway in the Pathogenesis and Treatment of Diabetic Foot: A Review.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. 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

7 authors at 2 institutions in 1 country.

Kyra Nicole LaubachComparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, CA 95616.
Wensheng YanComparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, CA 95616.
Xiangmudong KongComparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, CA 95616.
Wenqiang SunComparative Oncology Laboratory, Schools of Medicine and Veterinary 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
Jin ZhangComparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, CA 95616.
Xinbin ChenComparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, CA 95616.
University of California, Davis · USThe University of Texas Southwestern Medical Center · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI KC KENT LLOYD · 2002 to 2026
$84.9M
TRAINING IN COMPARATIVE LUNG BIOLOGY AND MEDICINET32HL007013 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI Elena Goncharova, Nicholas J. KENYON · 1985 to 2026
$10.1M
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
NCI NIH HHS P30 CA093373NCI NIH HHS R01 CA081237NCI NIH HHS R01 CA224433NHLBI NIH HHS T32 HL007013
6 · The paper itself

Abstract

p73, a p53 family member, undergoes alternative splicing at the 3′ end to produce multiple isoforms, but their expression and activity are largely unknown. Thus, CRISPR was used to knock out exon 12 (E12) in human cancer cell lines and mice, leading to isoform switch from p73α to isoform p73α1. We found that p73α1 is naturally expressed and induced by DNA damage. We also found that knockout of E12 suppresses cell growth and migration in H1299 and MIA PaCa-2 cells and promotes cellular senescence in mouse embryonic fibroblasts. Similarly, ectopic expression of p73α1 suppresses cell proliferation, whereas knockdown of p73α1 restores the cell proliferative and migratory capacities of E12

Indexed as

Genes, Tumor SuppressorInflammationNeoplasmsReceptor, Notch1Tumor Protein p73AnimalsCell Line, TumorDNA DamageExonsGene Knockout TechniquesHumansMiceMice, KnockoutProtein IsoformsProtein IsoformsReceptor, Notch1Tumor Protein p73Notch1 pathwayp53 familyp73p73 C-terminal isoformstumor suppressor

Identifiers

PMID35617425
PMCPMC9296871
OpenAlexW4281569328

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.