Evidence map›Paper›PMID 16547506›Full record

ArticleOncogene2006

Human polyomavirus BKV transcriptionally activates DNA methyltransferase 1 through the pRb/E2F pathway.

M T McCabe, J A Low, M J Imperiale, M L Day

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Influence of bacteria on epigenetic gene control.Cellular and molecular life sciences : CMLS · 2014
    Review
  11. Article
  12. Review
  13. Polyoma BK Virus: An Oncogenic Virus?Case reports in nephrology · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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.

M T McCabeProgram in Cellular and Molecular Biology, Department of Urology, University of Michigan, Ann Arbor, MI 48109-0944, USA.
J A Low
M J Imperiale
M L Day
University of Michigan–Ann Arbor · US

Funding

Training Program in Tumor MicroenvironmentT32CA009676 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Maria G Castro, Analisa Virginia DiFeo · 1992 to 2026
$7.3M
Parameters Governing Kidney Cell Infection with BKVR01AI060584 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI IMPERIALE, MICHAEL J. · 2004 to 2020
$4.8M
Role of Retinoblastoma in Prostate HomeostasisR01DK061488 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAY, MARK L · 2003 to 2006
$1.1M
NCI NIH HHS 5T32 CA09676NIAID NIH HHS AI060584NIDDK NIH HHS DK61488
6 · The paper itself

Abstract

Many DNA tumor virus oncogenes are capable of activating and highjacking the host cell's DNA replication machinery for its own reproduction purposes through targeting and inactivation of the retinoblastoma pocket protein family. Pocket proteins function to regulate cell cycle progression and DNA synthesis through inhibitory interactions with the E2F transcription factors. The interaction of viral oncogenes with the pocket proteins is crucial for their transforming activity. We recently demonstrated that the DNA methyltransferase 1 (DNMT1) gene is an E2F target gene that is transcriptionally activated in cells lacking the retinoblastoma gene (Rb-/-). Overexpression of DNMT1 is implicated in tumor suppressor gene hypermethylation which is associated with tumorigenesis. Given that viral oncogenes potently stimulate E2F activity, we hypothesized that viral infection might activate DNMT1 and thereby promote transformation. Herein, we demonstrate that DNMT1 is strongly activated by the human polyomavirus BKV large T antigen (TAg) and adenovirus E1a. Viral oncogene mutants incapable of binding the pocket proteins are ineffective at activating DNMT1 compared to their wild-type counterparts. Additionally, mutation of the E2F sites within the DNMT1 promoters dramatically abrogates transcriptional activation. These data suggest that viral induction of DNMT1 through modulation of the pRB/E2F pathway may be involved in viral transformation.

Indexed as

Cell Transformation, ViralSignal TransductionAdenocarcinomaAdenovirus E1A ProteinsAnimalsAntigens, Polyomavirus TransformingBK VirusCells, CulturedDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesE2F Transcription FactorsEmbryo, MammalianEnzyme ActivationFibroblastsHumansLuciferasesAdenovirus E1A ProteinsAntigens, Polyomavirus TransformingDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNMT1 protein, humanDnmt1 protein, mouseE2F Transcription FactorsLuciferasesRetinoblastoma ProteinRNA, Messenger

Identifiers

PMID16547506
OpenAlexW2036980797

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.