Evidence map›Paper›PMID 20739528›Full record

ArticleJournal of virology2010

NFX1 plays a role in human papillomavirus type 16 E6 activation of NFkappaB activity.

Mei Xu, Rachel A Katzenellenbogen, Carla Grandori, Denise A Galloway

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 42 citations in OpenAlex.

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  14. The scope of viral causation of human cancers: interpreting virus density from an evolutionary perspective.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
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  15. Article
  16. Article
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  18. The Interaction Between Human Papillomaviruses and the Stromal Microenvironment.Progress in molecular biology and translational science · 2016
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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 at 2 institutions in 1 country.

Mei XuFred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, C1-015, Seattle, WA 98109-1024, USA.
Rachel A Katzenellenbogen
Carla Grandori
Denise A Galloway
University of Washington · USFred Hutch Cancer Center · US

Funding

INTERACTIONS OF HPV ONCOGENES WITH THE P53 PATHWAYR01CA064795 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GALLOWAY, DENISE A. · 1995 to 2017
$8.6M
Regulation of Telomerase by NFX1K08CA131171 · NCI · SEATTLE CHILDREN'S HOSPITAL · PI KATZENELLENBOGEN, RACHEL ADRIA · 2008 to 2012
$672k
NCI NIH HHS R01 CA064795
6 · The paper itself

Abstract

High-risk human papillomavirus (HR HPV) requires differentiating epithelial cells to continue to divide in order to replicate the viral DNA. To achieve this, HPV perturbs several regulatory pathways, including cellular apoptosis and senescence signals. HPV E6 has been identified as a regulator of the NFκB signaling pathway, a pathway important in many cellular processes, as well as regulation of virus-host cell interactions. We report here that NFX1-91, an endogenously expressed transcriptional regulator of human telomerase reverse transcriptase (hTERT) that is targeted by HPV type 16 (HPV16) E6/E6-associated protein (E6AP) for degradation, is also critical for regulation of the NFκB pathway by HPV16 E6. Microarray analysis revealed induction of NFκB-responsive genes and reduction of NFκB inhibitors with knockdown of NFX1-91. Knockdown of NFX1-91 induced downregulation of p105, an NFκB inhibitor in both primary human foreskin keratinocytes (HFKs) and HCT116 cells. Chromatin immunoprecipitation assays further confirmed that NFX1-91 bound to the p105 promoter and upregulated its expression. Similarly, in HPV16 E6-positive cells, reduction of p105 expression was observed, paralleling knockdown of NFX1-91 expression. Overall, our data suggest a mechanism for HPV16 E6 activation of the NFκB pathway through NFX1-91. Also, it provides evidence that NFX1-91 can function as a dual regulator, not only a transcriptional repressor, but also a transcriptional activator, when bound to DNA.

Indexed as

Cells, CulturedHumansKeratinocytesMicroarray AnalysisNF-kappa BNF-kappa B p50 SubunitOncogene Proteins, ViralPromoter Regions, GeneticRepressor ProteinsTranscriptional ActivationTranscription FactorsE6 protein, Human papillomavirus type 16NF-kappa BNF-kappa B p50 SubunitNFKB1 protein, humanNFX1 protein, humanOncogene Proteins, ViralRepressor ProteinsTranscription Factors

Identifiers

PMID20739528
PMCPMC2953198
OpenAlexW2161245668

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.