Evidence map›Paper›PMID 15856010›Full record

ArticleOncogene2005

Crosstalk between the human papillomavirus E2 transcriptional activator and the E6 oncoprotein.

Helena Sterlinko Grm, Paola Massimi, Noor Gammoh, Lawrence Banks

Abstract read
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In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

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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

4 authors.

Helena Sterlinko GrmInternational Centre for Genetic Engineering and Biotechnology, Padriciano 99, 34012 Trieste, Italy.
Paola Massimi
Noor Gammoh
Lawrence Banks

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human papillomaviruses are the causative agents of cervical cancer. Previous studies have shown that loss of the viral E2 protein during malignant progression is an important feature of HPV-induced malignancy due to the resulting uncontrolled expression of the viral oncoproteins E6 and E7. We now show however that the viral E2 and E6 proteins are both capable of regulating each other's activity. When coexpressed, E2 and E6 induce marked changes in the pattern of each other's expression, with preferential accumulation in nuclear speckles. The two proteins interact directly, resulting in changes in the substrate specificities of E6 and the biochemical activities of E2. Thus, while E6 efficiently degrades its PDZ domain-containing substrates in the absence of E2, this activity is greatly diminished when E2 is present. Likewise, E2 alone drives both viral DNA replication and viral gene expression. However, in the presence of E6, viral DNA replication is inhibited while the transcriptional activity of E2 is elevated. These studies define a far more complex pattern of interaction between E2 and E6 than was previously thought and redefines the possible consequences of loss of E2 with respect to uncontrolled E6 activity and consequent malignant progression.

Indexed as

Cells, CulturedCell Transformation, NeoplasticCell Transformation, ViralDNA-Binding ProteinsDNA ReplicationDNA, ViralGene Expression Regulation, ViralHumansOncogene Proteins, ViralPapillomaviridaeProtein BindingRecombinant Fusion ProteinsRepressor ProteinsTranscription FactorsTumor Cells, CulturedDNA-Binding ProteinsDNA, ViralE2 protein, Human papillomavirus type 16E6 protein, Human papillomavirus type 16E6 protein, Human papillomavirus type 18Oncogene Proteins, ViralRecombinant Fusion ProteinsRepressor ProteinsTranscription Factors

Identifiers

PMID15856010

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.