Evidence map›Paper›PMID 30692643›Full record

ArticleCell death and differentiation2019

Fam83F induces p53 stabilisation and promotes its activity.

Mohammed Salama, Diego Benitez-Riquelme, Seham Elabd, Leonel Munoz, Ping Zhang, Matthias Glanemann, Maria Caterina Mione, Robert Goldin, Thierry Soussi, Gary Davidson and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 42 citations in OpenAlex.

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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

11 authors at 3 institutions in 8 countries.

Mohammed SalamaKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, PO-box 3640, 76021, Karlsruhe, Germany.
Diego Benitez-RiquelmeKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, PO-box 3640, 76021, Karlsruhe, Germany.
Seham ElabdKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, PO-box 3640, 76021, Karlsruhe, Germany.
Leonel MunozKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, PO-box 3640, 76021, Karlsruhe, Germany.
Ping ZhangKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, PO-box 3640, 76021, Karlsruhe, Germany.
Matthias GlanemannKlinik fuer Allgemeine Chirurgie, Universitaetsklinikum des Saarlandes, Kirrberger Str., 66421, Homburg, Germany.
Maria Caterina MioneKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, PO-box 3640, 76021, Karlsruhe, Germany.ORCID http://orcid.org/0000-0002-9040-3705
Robert GoldinDepartment of Cellular Pathology, Clarence Wing, St. Mary's Campus, London, UK.
Thierry SoussiSorbonne Université, UPMC Univ Paris 06, F-75005, Paris, France.
Gary DavidsonKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, PO-box 3640, 76021, Karlsruhe, Germany.
Christine BlattnerKarlsruhe Institute of Technology, Institute of Toxicology and Genetics, PO-box 3640, 76021, Karlsruhe, Germany. christine.blattner@kit.edu.ORCID http://orcid.org/0000-0002-7250-5273
Karlsruhe Institute of Technology · DEInserm · FRUniversitätsklinikum des Saarlandes · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53 is one of the most important tumour suppressor proteins currently known. It is activated in response to DNA damage and this activation leads to proliferation arrest and cell death. The abundance and activity of p53 are tightly controlled and reductions in p53's activity can contribute to the development of cancer. Here, we show that Fam83F increases p53 protein levels by protein stabilisation. Fam83F interacts with p53 and decreases its ubiquitination and degradation. Fam83F is induced in response to DNA damage and its overexpression also increases p53 activity in cell culture experiments and in zebrafish embryos. Downregulation of Fam83F decreases transcription of p53 target genes in response to DNA damage and increases cell proliferation, identifying Fam83F as an important regulator of the DNA damage response. Overexpression of Fam83F also enhances migration of cells harbouring mutant p53 demonstrating that it can also activate mutant forms of p53.

Indexed as

Cell Line, TumorCell ProliferationHumansIntracellular Signaling Peptides and ProteinsNeoplasm ProteinsTumor Suppressor Protein p53FAM83F protein, humanIntracellular Signaling Peptides and ProteinsNeoplasm ProteinsTumor Suppressor Protein p53

Identifiers

PMID30692643
PMCPMC6748130
OpenAlexW2914456782

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.