Evidence map›Paper›PMID 30894485›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

PTPN14 degradation by high-risk human papillomavirus E7 limits keratinocyte differentiation and contributes to HPV-mediated oncogenesis.

Joshua Hatterschide, Amelia E Bohidar, Miranda Grace, Tara J Nulton, Hee Won Kim, Brad Windle, Iain M Morgan, Karl Munger, Elizabeth A White

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 111 citations in OpenAlex.

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  17. HPV Infections-Classification, Pathogenesis, and Potential New Therapies.International journal of molecular sciences · 2024
    Review
  18. HPV18 E7 inhibits LATS1 kinase and activates YAP1 by degrading PTPN14.bioRxiv : the preprint server for biology · 2024
    Article
  19. Review
  20. Article

6 more citing papers are in PubMed but not listed here.

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.

Joshua HatterschideDepartment of Otorhinolaryngology: Head and Neck Surgery, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104.
Amelia E BohidarDepartment of Otorhinolaryngology: Head and Neck Surgery, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104.
Miranda GraceDepartment of Developmental, Molecular, and Chemical Biology, Tufts University School of Medicine, Boston, MA 02111.
Tara J NultonPhilips Institute for Oral Health Research, Department of Oral and Craniofacial Molecular Biology, Virginia Commonwealth University School of Dentistry, Richmond, VA 23298.
Hee Won KimDepartment of Otorhinolaryngology: Head and Neck Surgery, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104.
Brad WindlePhilips Institute for Oral Health Research, Department of Oral and Craniofacial Molecular Biology, Virginia Commonwealth University School of Dentistry, Richmond, VA 23298.
Iain M MorganPhilips Institute for Oral Health Research, Department of Oral and Craniofacial Molecular Biology, Virginia Commonwealth University School of Dentistry, Richmond, VA 23298.
Karl MungerDepartment of Developmental, Molecular, and Chemical Biology, Tufts University School of Medicine, Boston, MA 02111.
Elizabeth A WhiteDepartment of Otorhinolaryngology: Head and Neck Surgery, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104; eawhite@pennmedicine.upenn.edu.
University of Pennsylvania · USVirginia Commonwealth University · USTufts University · US

Funding

BIOLOGICAL ACTIVITY OF HPV E7 IN HUMAN EPITHELIAL CELLSR01CA066980 · NCI · TUFTS UNIVERSITY BOSTON · PI MUNGER, KARL · 1996 to 2019
$7.4M
NCI NIH HHS R01 CA066980
6 · The paper itself

Abstract

High-risk human papillomavirus (HPV) E7 proteins enable oncogenic transformation of HPV-infected cells by inactivating host cellular proteins. High-risk but not low-risk HPV E7 target PTPN14 for proteolytic degradation, suggesting that PTPN14 degradation may be related to their oncogenic activity. HPV infects human keratinocytes but the role of PTPN14 in keratinocytes and the consequences of PTPN14 degradation are unknown. Using an HPV16 E7 variant that can inactivate retinoblastoma tumor suppressor (RB1) but cannot degrade PTPN14, we found that high-risk HPV E7-mediated PTPN14 degradation impairs keratinocyte differentiation. Deletion of

Indexed as

Cell DifferentiationCell Transformation, ViralProteolysisCell LineCell SurvivalGene Expression RegulationHuman papillomavirus 16HumansKeratinocytesPapillomavirus E7 ProteinsProtein Tyrosine Phosphatases, Non-ReceptorRetinoblastoma Binding ProteinsUbiquitin-Protein Ligasesoncogene protein E7, Human papillomavirus type 16Papillomavirus E7 ProteinsProtein Tyrosine Phosphatases, Non-ReceptorPTPN14 protein, humanRB1 protein, humanRetinoblastoma Binding ProteinsUbiquitin-Protein LigasescarcinogenesisdifferentiationHPVpapillomavirusPTPN14

Identifiers

PMID30894485
PMCPMC6452706
OpenAlexW2901712298

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.