Evidence map›Paper›PMID 18815281›Full record

ArticleBlood2009

Epstein-Barr virus latent membrane protein 2A exploits Notch1 to alter B-cell identity in vivo.

Leah J Anderson, Richard Longnecker

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Epstein-Barr virus latent genes.Experimental & molecular medicine · 2015
    Review
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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

2 authors at 1 institution in 1 country.

Leah J AndersonDepartment of Microbiology and Immunology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Avenue, Chicago, IL 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
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
Training Program in Viral ReplicationT32AI060523 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LAIMINS, LAIMONIS A. · 2004 to 2013
$1.4M
NCI NIH HHS CA 62234NCI NIH HHS CA 73507NCI NIH HHS R01 CA062234NCI NIH HHS R01 CA073507NIAID NIH HHS AI 067048NIAID NIH HHS R01 AI067048NIAID NIH HHS T32 AI 060523NIAID NIH HHS T32 AI060523
6 · The paper itself

Abstract

Expression of latent membrane protein 2 (LMP2A) during B-cell development leads to global alterations in gene transcription similar to those seen in Hodgkin Reed-Sternberg cells of Hodgkin lymphoma (HL). Along with the consistent detection of LMP2A in Epstein-Barr virus-associated HL, this implicates a role for LMP2A in the pathogenesis of HL. We have shown that LMP2A constitutively activates the Notch1 pathway to autoregulate the LMP2A promoter. To determine whether constitutive activation of the Notch pathway is important for LMP2A-mediated alterations in B-cell development in vivo, TgE-LMP2A-transgenic mice were intercrossed with mice expressing loxP-flanked Notch1 genes and Cre recombinase. B cells from TgE Notch1(lox/lox)-CD19(+/Cre) mice have an increase in immunoglobulin M and CD43 and a decrease in CD5 expression in the bone marrow compared with TgE Notch1(lox/lox) mice, indicating the LMP2A signal for developmental aberrations is impaired in the absence of Notch1. Real-time reverse-transcribed polymerase chain reaction analysis reveals that LMP2A requires the Notch1 pathway to alter levels of B cell-specific transcription factors, E2A and EBF. Interestingly, Notch1 appears to be important for LMP2A-mediated survival in low interleukin-7. We propose that LMP2A and the Notch1 pathway may cooperate to induce the alterations in B-cell identity seen in Hodgkin Reed-Sternberg cells.

Indexed as

AnimalsAntigens, CD19B-LymphocytesBone Marrow CellsCell SurvivalEpstein-Barr Virus InfectionsFlow CytometryHerpesvirus 4, HumanImmunoglobulin MLeukosialinMiceMice, Inbred C57BLMice, TransgenicReceptor, Notch1Reed-Sternberg CellsSignal TransductionAntigens, CD19EBV-associated membrane antigen, Epstein-Barr virusImmunoglobulin MLeukosialinNotch1 protein, mouseReceptor, Notch1Spn protein, mouseViral Matrix Proteins

Identifiers

PMID18815281
PMCPMC2614628
OpenAlexW1977912281

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.