Evidence map›Paper›PMID 21258403›Full record

ArticleOncogene2011

EAPP: gatekeeper at the crossroad of apoptosis and p21-mediated cell-cycle arrest.

P Andorfer, H Rotheneder

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  8. Article
  9. Mechanisms of radiation toxicity in transformed and non-transformed cells.International journal of molecular sciences · 2013
    Review
  10. EAPP modulates the activity of p21 and Chk2.Cell cycle (Georgetown, Tex.) · 2011
    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

2 authors at 2 institutions in 1 country.

P AndorferMax F. Perutz Laboratories, Department of Medical Biochemistry, Medical University of Vienna, Vienna, Austria.
H Rotheneder
Max Perutz Labs · ATMedical University of Vienna · AT

Funding

Austrian Science Fund FWF P 18417
6 · The paper itself

Abstract

We previously identified and characterized E2F-associated phospho-protein (EAPP), a nuclear phosphoprotein that interacts with the activating members of the E2F transcription factor family. EAPP levels are frequently elevated in transformed human cells. To examine the biological relevance of EAPP, we studied its properties in stressed and unstressed cells. Overexpression of EAPP in U2OS cells increased the fraction of G1 cells and lead to heightened resistance against DNA damage- or E2F1-induced apoptosis in a p21-dependent manner. EAPP itself becomes upregulated in confluent cells and after DNA damage and stimulates the expression of p21 independently of p53. It binds to the p21 promoter and seems to be required for the assembly of the transcription initiation complex. RNAi-mediated knockdown of EAPP expression brought about increased sensitivity towards DNA damage and resulted in apoptosis even in the absence of stress. Our results indicate that the level of EAPP is critical for cellular homeostasis. Too much of it results in G1 arrest and resistance to apoptosis, which, paradoxically, might favor cellular transformation. Too little EAPP seems to retard the expression not only of the p21 gene, but also of a number of other genes and ultimately results in apoptosis.

Indexed as

ApoptosisCell CycleBinding SitesBlotting, WesternCell Line, TumorCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsDNA DamageE2F1 Transcription FactorFlow CytometryG1 PhaseGene Expression Regulation, NeoplasticGreen Fluorescent ProteinsHumansPromoter Regions, GeneticProtein BindingCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsE2F1 protein, humanE2F1 Transcription FactorEAPP protein, humanGreen Fluorescent ProteinsSp1 Transcription FactorTranscription Factors

Identifiers

PMID21258403
PMCPMC3114185
OpenAlexW1967205171

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.