Evidence map›Paper›PMID 20849854›Full record

ArticleFEBS letters2010

Overexpression of SCYL1-BP1 stabilizes functional p53 by suppressing MDM2-mediated ubiquitination.

Jing Yan, Yujun Di, Huili Shi, Hai Rao, Keke Huo

Abstract read
In one paragraph

Article in FEBS letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-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

15 citing papers in PubMed, 19 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

5 authors at 2 institutions in 2 countries.

Jing YanState Key Laboratory of Genetic Engineering, Fudan University, Shanghai, China.
Yujun Di
Huili Shi
Hai Rao
Keke Huo
Fudan University · CNThe University of Texas Health Science Center at San Antonio · US

Funding

Targeting ubiquitylated proteins to the proteasomeR01GM078085 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI RAO, HAI · 2007 to 2011
$1.3M
NIGMS NIH HHS R01 GM078085
6 · The paper itself

Abstract

Previously, we defined SCY1-like 1 binding protein 1 (SCYL1-BP1) to be a substrate of Pirh2 that binds to mouse double minute gene number 2 (MDM2). In the current study, we found that an increase in SCYL1-BP1 protein levels caused a parallel change in the amount of p53 protein due to the inhibition by SCYL-BP1 of MDM2-mediated p53 ubiquitination. SCYL1-BP1 was not able to alter the ubiquitination of p53 by human papillomavirus protein E6, indicating that the effect was specific for MDM2. Increases in the level of SCYL1-BP1 protein in cells led to the greater transcriptional activation of p21 and gadd45, reduced rate of cellular proliferation, increased levels of apoptosis and inhibition of tumorigenicity. Thus, we propose that SCYL1-BP1 is a novel regulator of the MDM2-p53 feedback loop and that it may be a potential tumor suppressor.

Indexed as

UbiquitinationAnimalsApoptosisBlotting, WesternCarrier ProteinsCell LineCell Line, TumorCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p21GADD45 ProteinsGolgi Matrix ProteinsGreen Fluorescent ProteinsHep G2 CellsHumansIntracellular Signaling Peptides and ProteinsCarrier ProteinsCyclin-Dependent Kinase Inhibitor p21GADD45 ProteinsGolgi Matrix ProteinsGORAB protein, humanGreen Fluorescent ProteinsIntracellular Signaling Peptides and ProteinsLuciferasesProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53

Identifiers

PMID20849854
PMCPMC3789512
OpenAlexW2030084060

What OpenQuestion holds

Textmetadata
LicenceTDM
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.