Evidence map›Paper›PMID 17980397›Full record

ArticleVirology2008

An auto-regulatory loop for EBV LMP2A involves activation of Notch.

Leah J Anderson, Richard Longnecker

Open access · greenAbstract read
In one paragraph

Article in Virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Epstein-Barr virus LMP2A imposes sensitivity to apoptosis.The Journal of general virology · 2010
    Article
  11. Article
  12. Article
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  14. Article
  15. Review
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

2 authors at 1 institution in 1 country.

Leah J AndersonDepartment of Microbiology and Immunology, Northwestern University, Chicago, Illinois 60611, USA.
Richard Longnecker
Northwestern University · US

Funding

In Vivo Model of Epstein-Barr Virus LatencyR01CA073507 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 1997 to 2018
$6.1M
Inhibitors of the Epstein-Barr Virus Entry MachineryR01CA117794 · NCI · STANFORD UNIVERSITY · PI JARDETZKY, THEODORE S, LONGNECKER, RICHARD M · 2006 to 2016
$3.0M
EBV LATENT MEMBRANE PROTEIN 2R01CA062234 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 1994 to 2007
$2.2M
EBV gB Function in Viral Fusion, Entry, and EgressR01AI067048 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 2007 to 2011
$1.9M
Functional Studies of gp42 and HLA Class 11 in EBVR01CA093444 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 2002 to 2006
$1.8M
Training Program in Viral ReplicationT32AI060523 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LAIMINS, LAIMONIS A. · 2004 to 2013
$1.4M
NCI NIH HHS CA117794NCI NIH HHS CA62234NCI NIH HHS CA73507NCI NIH HHS CA93444NCI NIH HHS R01 CA062234NCI NIH HHS R01 CA073507NCI NIH HHS R01 CA093444NCI NIH HHS R01 CA117794NIAID NIH HHS AI067048NIAID NIH HHS R01 AI067048NIAID NIH HHS T32 AI060523
6 · The paper itself

Abstract

LMP2A is consistently detected in Hodgkin's lymphoma, nasopharyngeal carcinoma and has also been detected in Burkitt's lymphoma. Interestingly, LMP2A is detected in the absence of the transcriptional activator EBNA2, suggesting that an alternative mechanism is responsible for LMP2A expression. The intracellular domain of Notch (Notch-IC) and EBNA2 are functional homologs and recent microarray analysis indicates that LMP2A may constitutively activate the Notch pathway in vivo. Coupled with evidence that Notch-IC can bind to and activate the LMP2A promoter, we hypothesized that expression of LMP2A results in the constitutive activation of the Notch pathway to auto-regulate its promoter. Our data indicate that LMP2A constitutively activates the Notch pathway in B cells and epithelial cells. Expression of LMP2A alone is sufficient to activate its own expression and the amino-terminal signaling domain is required as LMP2B is unable to activate the LMP2A promoter. In addition, point mutations in tyrosines 31, 101 and 112 each results in a significant decrease in LMP2A promoter activation. Deletion of the RBP-Jkappa consensus sequences results in a significant decrease in promoter activity. The observation that LMP2A activates its own promoter suggests that LMP2A exploits the Notch pathway in order to control its own expression and may explain EBNA2-independent expression of LMP2A in EBV-associated malignancies.

Indexed as

Gene Expression RegulationGene Expression Regulation, ViralB-LymphocytesCell LineCell Line, TumorEpithelial CellsGene DeletionHerpesvirus 4, HumanHumansPoint MutationPromoter Regions, GeneticReceptor, Notch1TransfectionViral Matrix ProteinsEBV-associated membrane antigen, Epstein-Barr virusNOTCH1 protein, humanReceptor, Notch1Viral Matrix Proteins

Identifiers

PMID17980397
PMCPMC2288488
OpenAlexW2092862007

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.