Evidence map›Paper›PMID 16381817›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

The E7 proteins of low- and high-risk human papillomaviruses share the ability to target the pRB family member p130 for degradation.

Benyue Zhang, Wei Chen, Ann Roman

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 4% 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

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 181 citations in OpenAlex.

  1. Pooled it
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  12. Genome composition-based deep learning predicts oncogenic potential of HPVs.Frontiers in cellular and infection microbiology · 2024
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50 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

3 authors at 2 institutions in 1 country.

Benyue ZhangDepartment of Microbiology and Immunology and The Walther Oncology Center, Indiana University School of Medicine and The Walther Cancer Institute, Indianapolis, IN 46202, USA.
Wei Chen
Ann Roman
Walther Cancer Foundation · USIndiana University – Purdue University Indianapolis · US

Funding

The Mechanisms of Human Papillomavirus PathogenicityR01AI049254 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI ROMAN, ANN · 2003 to 2006
$1.2M
NIAID NIH HHS AI49254NIAID NIH HHS R01 AI049254
6 · The paper itself

Abstract

High-risk human papillomaviruses (HPVs) (e.g., HPV-16) cause anogenital and head and neck cancers, and low-risk HPVs (e.g., HPV-6) cause benign hyperproliferative disease. The E7 protein of HPV-16 binds all retinoblastoma tumor suppressor protein (pRB) family members with higher affinity than HPV-6E7. The HPV-16 E7 protein has been reported to target pRB family members for degradation and to immortalize cells. Here we tested the hypothesis that the low-risk E7 protein has an intrinsic ability to decrease expression of pRB family members. First, we introduced a high-affinity pRB-binding site into HPV-6 E7 (6E7G22D) and showed that, in human foreskin keratinocytes, HPV-6 E7G22D decreased the level of pRB protein but not pRB mRNA. Second, we analyzed the ability of wild-type HPV-6 E7 to destabilize the other pRB family members, p107 and p130. HPV-6 E7, like HPV-16 E7, decreased the level of p130 protein. This decrease was inhibited by MG132, a proteasome inhibitor. Binding of HPV-6 E7 to p130 was necessary but not sufficient to decrease the level of p130. Furthermore, the destabilization of p130 correlated with a decrease in the expression of involucrin, a differentiation marker. We suggest that the shared activity of HPV-16 E7 and HPV-6 E7 to destabilize p130 and decrease or delay differentiation may be related to the role of E7 in the HPV life cycle. The added ability of HPV-16 E7 to regulate pRB and p107 may be related to oncogenic activity.

Indexed as

Amino Acid SequenceBinding SitesCell DifferentiationCells, CulturedCulture MediaHumansKeratinocytesMolecular Sequence DataOncogene Proteins, ViralPapillomaviridaePapillomavirus E7 ProteinsProteasome Endopeptidase ComplexRetinoblastoma-Like Protein p130Risk FactorsCulture Mediaoncogene protein E7, Human papillomavirus type 16oncogene protein E7, Human papillomavirus type 6Oncogene Proteins, ViralPapillomavirus E7 ProteinsProteasome Endopeptidase ComplexRetinoblastoma-Like Protein p130

Identifiers

PMID16381817
PMCPMC1326189
OpenAlexW1977746653

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.