Evidence map›Paper›PMID 31107240›Full record

ArticleeLife2019

ADAM17-dependent signaling is required for oncogenic human papillomavirus entry platform assembly.

Snježana Mikuličić, Jérôme Finke, Fatima Boukhallouk, Elena Wüstenhagen, Dominik Sons, Yahya Homsi, Karina Reiss, Thorsten Lang, Luise Florin

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 37 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

9 authors at 3 institutions in 1 country.

Snježana MikuličićInstitute for Virology and Research Center for Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Jérôme FinkeDepartment of Membrane Biochemistry, Life and Medical Sciences Institute (LIMES), University of Bonn, Bonn, Germany.
Fatima BoukhalloukInstitute for Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Elena WüstenhagenInstitute for Virology and Research Center for Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.ORCID 0000-0002-5420-6536
Dominik SonsDepartment of Membrane Biochemistry, Life and Medical Sciences Institute (LIMES), University of Bonn, Bonn, Germany.
Yahya HomsiDepartment of Membrane Biochemistry, Life and Medical Sciences Institute (LIMES), University of Bonn, Bonn, Germany.
Karina ReissDepartment of Dermatology and Allergology, University Hospital Schleswig-Holstein, Kiel, Germany.
Thorsten LangDepartment of Membrane Biochemistry, Life and Medical Sciences Institute (LIMES), University of Bonn, Bonn, Germany.ORCID 0000-0002-9128-0137
Luise FlorinInstitute for Virology and Research Center for Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.ORCID 0000-0003-4310-7329
Johannes Gutenberg University Mainz · DEUniversity of Bonn · DEUniversity Hospital Schleswig-Holstein · DE

Funding

Deutsche Forschungsgemeinschaft CRC877 (A4)Deutsche Forschungsgemeinschaft FL 696/3-1Deutsche Forschungsgemeinschaft LA 1272/8-1Deutsche Forschungsgemeinschaft LA 1272/8-1, FL 696/3-1
6 · The paper itself

Abstract

Oncogenic human papillomaviruses (HPV) are small DNA viruses that infect keratinocytes. After HPV binding to cell surface receptors, a cascade of molecular interactions mediates the infectious cellular internalization of virus particles. Aside from the virus itself, important molecular players involved in virus entry include the tetraspanin CD151 and the epidermal growth factor receptor (EGFR). To date, it is unknown how these components are coordinated in space and time. Here, we studied plasma membrane dynamics of CD151 and EGFR and the HPV16 capsid during the early phase of infection. We find that the proteinase ADAM17 activates the extracellular signal-regulated kinases (ERK1/2) pathway by the shedding of growth factors which triggers the formation of an endocytic entry platform. Infectious endocytic entry platforms carrying virus particles consist of two-fold larger CD151 domains containing the EGFR. Our finding clearly dissects initial virus binding from ADAM17-dependent assembly of a HPV/CD151/EGFR entry platform.

Indexed as

ADAM17 ProteinCarcinogenesisCell MembraneEndocytosisErbB ReceptorsHeLa CellsHuman papillomavirus 16HumansKeratinocytesMAP Kinase Signaling SystemPapillomaviridaePapillomavirus InfectionsTetraspanin 24VirionVirus InternalizationADAM17 ProteinADAM17 protein, humanCD151 protein, humanEGFR protein, humanErbB ReceptorsTetraspanin 24ADAM17cell biologyentry receptor complexgrowth factorshumaninfectious diseasemicrobiologymicrodomainsoncogenic Papillomavirustetraspanin

Identifiers

PMID31107240
PMCPMC6557631
OpenAlexW2946652169

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.