Evidence map›Paper›PMID 18321970›Full record

ArticleJournal of virology2008

Casein kinase II motif-dependent phosphorylation of human papillomavirus E7 protein promotes p130 degradation and S-phase induction in differentiated human keratinocytes.

Nicholas J Genovese, N Sanjib Banerjee, Thomas R Broker, Louise T Chow

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  7. Review
  8. Oncogenic HPV promotes the expression of the long noncoding RNA lnc-FANCI-2 through E7 and YY1.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Article
  10. Targeting DNA Damage Response as a Strategy to Treat HPV Infections.International journal of molecular sciences · 2019
    Article
  11. Article
  12. Vorinostat, a pan-HDAC inhibitor, abrogates productive HPV-18 DNA amplification.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
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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 1 institution in 1 country.

Nicholas J GenoveseUniversity of Alabama at Birmingham, Biochemistry and Molecular Genetics, 1918 University Boulevard, McCallum Building 510, Birmingham, AL 35294-0005, USA.
N Sanjib Banerjee
Thomas R Broker
Louise T Chow
University of Alabama at Birmingham · US

Funding

MECHANISMS OF HUMAN PAPILLOMAVIRUS DNA REPLICATIONR01CA083679 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHOW, LOUISE T · 1999 to 2015
$5.1M
BASIC MECHANISMS IN AIDS PATHOGENESIST32AI007493 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MORROW, CASEY D · 1995 to 2014
$4.2M
NCI NIH HHS CA83679NCI NIH HHS R01 CA083679NIAID NIH HHS T32 AI007493NIAID NIH HHS T32 AI07493
6 · The paper itself

Abstract

The E7 proteins of human papillomaviruses (HPVs) promote S-phase reentry in differentiated keratinocytes of the squamous epithelia to support viral DNA amplification. In this study, we showed that nuclear p130 was present in the differentiated strata of several native squamous epithelia susceptible to HPV infection. In contrast, p130 was below the level of detection in HPV-infected patient specimens. In submerged and organotypic cultures of primary human keratinocytes, the E7 proteins of the high-risk mucosotrophic HPV-18, the benign cutaneous HPV-1, and, to a lesser extent, the low-risk mucosotropic HPV-11 destabilized p130. This E7 activity depends on an intact pocket protein binding domain and a casein kinase II (CKII) phosphorylation motif. Coimmunoprecipitation experiments showed that both E7 domains were important for binding to p130 in extracts of organotypic cultures. Metabolic labeling in vivo demonstrated that E7 proteins were indeed phosphorylated in a CKII motif-dependent manner. Moreover, the efficiencies of the E7 proteins of various HPV types or mutations to induce S-phase reentry in spinous cells correlated with their relative abilities to bind and to destabilize p130. Collectively, these data support the notion that p130 controls the homeostasis of the differentiated keratinocytes and is therefore targeted by E7 for degradation to establish conditions permissive for viral DNA amplification.

Indexed as

Cell CycleAmino Acid SequenceCells, CulturedEpitheliumHuman papillomavirus 11Human papillomavirus 18HumansKeratinocytesMolecular Sequence DataPapillomaviridaePapillomavirus E7 ProteinsPhosphorylationProtein BindingProtein Interaction MappingProtein Structure, TertiaryRetinoblastoma-Like Protein p130Papillomavirus E7 ProteinsRetinoblastoma-Like Protein p130

Identifiers

PMID18321970
PMCPMC2346766
OpenAlexW2144240071

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.