Evidence map›Paper›PMID 36897777›Full record

ArticleCell reports2023

FAM193A is a positive regulator of p53 activity.

Maria M Szwarc, Anna L Guarnieri, Molishree Joshi, Huy N Duc, Madison C Laird, Ahwan Pandey, Santosh Khanal, Emily Dohm, Aimee K Bui, Kelly D Sullivan and 3 more

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

Article in Cell reports, 2023. 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
1.6field-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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  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

13 authors at 2 institutions in 2 countries.

Maria M SzwarcDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Anna L GuarnieriDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Molishree JoshiDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Functional Genomics Facility, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Huy N DucFunctional Genomics Facility, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Madison C LairdFunctional Genomics Facility, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Ahwan PandeyDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia.
Santosh KhanalDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Emily DohmDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Aimee K BuiDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Kelly D SullivanDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Pediatrics, Section of Developmental Biology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Matthew D GalbraithDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Zdenek AndrysikDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA. Electronic address: zdenek.andrysik@cuanschutz.edu.
Joaquin M EspinosaDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Functional Genomics Facility, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA. Electronic address: joaquin.espinosa@cuanschutz.edu.
University of Colorado Anschutz Medical Campus · USPeter MacCallum Cancer Centre · AU

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
University of Colorado Anschutz Medical Campus DRCP30DK116073 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI LORI SUSSEL · 2020 to 2026
$10.8M
ZEBRAFISH TRANSGENIC CORE - ROCKY MOUNTAIN NEUROLOGICAL DISORDERS CORE CENTERP30NS048154 · NINDS · UNIVERSITY OF COLORADO DENVER · PI RIBERA, ANGELES BADELL · 2004 to 2020
$10.1M
Stress- and Promoter-Specific Mechanisms of Transcritpional Activation by p53R01CA117907 · NCI · UNIVERSITY OF COLORADO DENVER · PI ESPINOSA, JOAQUIN M. · 2006 to 2022
$4.4M
NCI NIH HHS P30 CA046934NCI NIH HHS R01 CA117907NIDDK NIH HHS P30 DK116073NINDS NIH HHS P30 NS048154
6 · The paper itself

Abstract

Inactivation of the p53 tumor suppressor, either by mutations or through hyperactivation of repressors such as MDM2 and MDM4, is a hallmark of cancer. Although many inhibitors of the p53-MDM2/4 interaction have been developed, such as Nutlin, their therapeutic value is limited by highly heterogeneous cellular responses. We report here a multi-omics investigation of the cellular response to MDM2/4 inhibitors, leading to identification of FAM193A as a widespread regulator of p53 function. CRISPR screening identified FAM193A as necessary for the response to Nutlin. FAM193A expression correlates with Nutlin sensitivity across hundreds of cell lines. Furthermore, genetic codependency data highlight FAM193A as a component of the p53 pathway across diverse tumor types. Mechanistically, FAM193A interacts with MDM4, and FAM193A depletion stabilizes MDM4 and inhibits the p53 transcriptional program. Last, FAM193A expression is associated with better prognosis in multiple malignancies. Altogether, these results identify FAM193A as a positive regulator of p53.

Indexed as

Antineoplastic AgentsNeoplasmsApoptosisAutoantigensCell Cycle ProteinsCell Line, TumorHumansProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Antineoplastic AgentsAutoantigensCell Cycle ProteinsFAM193A protein, humanMDM4 protein, humanProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53apoptosiscell-cycle arrestCP: CancerCP: Molecular biologyCRISPRMDM2MDM4MDMXNutlinp53

Identifiers

PMID36897777
PMCPMC10164416
OpenAlexW4323666010

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.