Evidence map›Paper›PMID 30903928›Full record

ArticleVirology2019

HPV type 16 E6 and NFX1-123 augment JNK signaling to mediate keratinocyte differentiation and L1 expression.

Justine Levan, Portia A Vliet-Gregg, Kristin L Robinson, Lisa R Matsumoto, Rachel A Katzenellenbogen

Open access · greenAbstract read
In one paragraph

Article in Virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 10 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

5 authors at 2 institutions in 1 country.

Justine LevanSeattle Children's Research Institute, Center for Global Infectious Disease Research, Seattle, WA, USA; Department of Global Health, Pathobiology Program, University of Washington, Seattle, WA, USA.
Portia A Vliet-GreggSeattle Children's Research Institute, Center for Global Infectious Disease Research, Seattle, WA, USA.
Kristin L RobinsonSeattle Children's Research Institute, Center for Global Infectious Disease Research, Seattle, WA, USA.
Lisa R MatsumotoSeattle Children's Research Institute, Center for Global Infectious Disease Research, Seattle, WA, USA.
Rachel A KatzenellenbogenSeattle Children's Research Institute, Center for Global Infectious Disease Research, Seattle, WA, USA; Department of Global Health, Pathobiology Program, University of Washington, Seattle, WA, USA; Department of Pediatrics, Division of Adolescent Medicine, University of Washington, Seattle WA, USA. Electronic address: rkatzene@iu.edu.
Infectious Disease Research Institute · USCenter for Infectious Disease Research · US

Funding

HPV E6 and NFX1-123 in differentiation, cell regulation, and cancerR01CA172742 · NCI · SEATTLE CHILDREN'S HOSPITAL · PI KATZENELLENBOGEN, RACHEL ADRIA · 2014 to 2024
$4.1M
Viral Pathogenesis Training ProgramT32AI083203 · NIAID · UNIVERSITY OF WASHINGTON · PI BLOOM, JESSE D, LAGUNOFF, MICHAEL · 2009 to 2023
$2.7M
NCI NIH HHS R01 CA172742NIAID NIH HHS T32 AI083203
6 · The paper itself

Abstract

The HPV life cycle is differentiation-dependent, with cellular differentiation driving initiation of the late, productive stage of the viral life cycle. Here, we identify a role for the protein NFX1-123 in regulating keratinocyte differentiation and events of the late HPV life cycle. NFX1-123 itself increased with differentiation of epithelial cells. Greater NFX1-123 augmented differentiation marker expression and JNK phosphorylation in differentiating 16E6-expressing human foreskin keratinocytes (16E6 HFKs). This was associated with altered expression of MKK4 and MKK7, upstream kinase regulators of JNK phosphorylation. Modulating levels of NFX1-123 in HPV16-positive W12E cells recapitulated the effects on differentiation markers, JNK phosphorylation, and MKK4/7 seen in 16E6 HFKs. Crucially, levels of NFX1-123 also correlated with expression of L1, the capsid protein of HPV. Altogether, these studies define a role for NFX1-123 in mediating epithelial differentiation through the JNK signaling pathway, potentially linking expression of cellular genes and HPV genes during differentiation.

Indexed as

Cell DifferentiationHuman papillomavirus 16HumansKeratinocytesMAP Kinase Kinase 4MAP Kinase Kinase KinasesMAP Kinase Signaling SystemOncogene Proteins, ViralPapillomavirus InfectionsRepressor ProteinsSignal TransductionE6 protein, Human papillomavirus type 16MAP Kinase Kinase 4MAP Kinase Kinase Kinasesmitogen-activated protein kinase kinase kinase 12NFX1 protein, humanOncogene Proteins, ViralRepressor ProteinsDifferentiationHR E6HR HPVKeratinocyteNFX1–123

Identifiers

PMID30903928
PMCPMC6486444
OpenAlexW2921765029

What OpenQuestion holds

Textmetadata
LicenceTDM
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.