Evidence map›Paper›PMID 27483446›Full record

ArticlePLoS pathogens2016

Analysis of Multiple HPV E6 PDZ Interactions Defines Type-Specific PDZ Fingerprints That Predict Oncogenic Potential.

Miranda Thomas, Michael P Myers, Paola Massimi, Corrado Guarnaccia, Lawrence Banks

Abstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed.

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  11. Viral subversion of the cell polarity regulator Scribble.Biochemical Society transactions · 2023
    Review
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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.

Miranda ThomasTumour Virology, International Centre for Genetic Engineering and Biotechnology (I.C.G.E.B.), Trieste, Italy.
Michael P MyersProtein Networks, International Centre for Genetic Engineering and Biotechnology (I.C.G.E.B.), Trieste, Italy.
Paola MassimiTumour Virology, International Centre for Genetic Engineering and Biotechnology (I.C.G.E.B.), Trieste, Italy.ORCID 0000-0002-8221-0399
Corrado GuarnacciaBiotechnology Development, International Centre for Genetic Engineering and Biotechnology (I.C.G.E.B.), Trieste, Italy.
Lawrence BanksTumour Virology, International Centre for Genetic Engineering and Biotechnology (I.C.G.E.B.), Trieste, Italy.

Funding

Wellcome TrustWellcome Trust 093450/B/10/Z
6 · The paper itself

Abstract

The high-risk Human Papillomavirus (HPV) E6 oncoproteins are characterised by the presence of a class I PDZ-binding motif (PBM) on their extreme carboxy termini. The PBM is present on the E6 proteins derived from all cancer-causing HPV types, but can also be found on some related non-cancer-causing E6 proteins. We have therefore been interested in investigating the potential functional differences between these different E6 PBMs. Using an unbiased proteomic approach in keratinocytes, we have directly compared the interaction profiles of these different PBMs. This has allowed us to identify the potential PDZ target fingerprints of the E6 PBMs from 7 different cancer-causing HPV types, from 3 HPV types with weak cancer association, and from one benign HPV type that possesses an ancestral PBM. We demonstrate a striking increase in the number of potential PDZ targets bound by each E6 PBM as cancer-causing potential increases, and show that the HPV-16 and HPV-18 PBMs have the most flexibility in their PDZ target selection. Furthermore, the specific interaction with hScrib correlates directly with increased oncogenic potential. In contrast, hDlg is bound equally well by all the HPV E6 PBMs analysed, indicating that this is an evolutionarily conserved interaction, and was most likely one of the original E6 PBM target proteins that was important for the occupation of a potential new niche. Finally, we present evidence that the cell junction components ZO-2 and β-2 syntrophin are novel PDZ domain-containing targets of a subset of high-risk HPV types.

Indexed as

CarcinogenesisCell LineHumansMass SpectrometryOncogene Proteins, ViralPapillomaviridaePDZ DomainsProteomicsOncogene Proteins, Viral

Identifiers

PMID27483446
PMCPMC4970744

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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.