Evidence map›Paper›PMID 28233861›Full record

ArticleScientific reports2017

Ubiquitin-specific peptidase 48 regulates Mdm2 protein levels independent of its deubiquitinase activity.

Kateřina Cetkovská, Hana Šustová, Stjepan Uldrijan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

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  11. Ubiquitin ligases: guardians of mammalian development.Nature reviews. Molecular cell biology · 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

3 authors at 1 institution in 1 country.

Kateřina CetkovskáDepartment of Biology, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Hana ŠustováDepartment of Biology, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Stjepan UldrijanDepartment of Biology, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Masaryk University · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The overexpression of Mdm2 has been linked to the loss of p53 tumour suppressor activity in several human cancers. Here, we present results suggesting that ubiquitin-specific peptidase 48 (USP48), a deubiquitinase that has been linked in previous reports to the NF-κB signaling pathway, is a novel Mdm2 binding partner that promotes Mdm2 stability and enhances Mdm2-mediated p53 ubiquitination and degradation. In contrast to other deubiquitinating enzymes (DUBs) that have been previously implicated in the regulation of Mdm2 protein stability, USP48 did not induce Mdm2 stabilization by significantly reducing Mdm2 ubiquitination levels. Moreover, two previously characterized USP48 mutants lacking deubiquitinase activity were also capable of efficiently stabilizing Mdm2, indicating that USP48 utilizes a non-canonical, deubiquitination-independent mechanism to promote Mdm2 oncoprotein stability. This study represents, to the best of our knowledge, the first report suggesting DUB-mediated target protein stabilization that is independent of its deubiquitinase activity. In addition, our results suggest that USP48 might represent a new mechanism of crosstalk between the NF-κB and p53 stress response pathways.

Indexed as

Gene Expression RegulationCell LineHumansProtein Processing, Post-TranslationalProteolysisProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53UbiquitinationUbiquitin-Specific ProteasesMDM2 protein, humanProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53Ubiquitin-Specific ProteasesUSP48 protein, human

Identifiers

PMID28233861
PMCPMC5324091
OpenAlexW2590154237

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.