Evidence map›Paper›PMID 16873269›Full record

ArticleJournal of virology2006

Epstein-Barr virus nuclear antigen 2 trans-activates the cellular antiapoptotic bfl-1 gene by a CBF1/RBPJ kappa-dependent pathway.

Pamela M Pegman, Sinéad M Smith, Brendan N D'Souza, Sinéad T Loughran, Sabine Maier, Bettina Kempkes, Paul A Cahill, Matthew J Simmons, Céline Gélinas, Dermot Walls

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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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

10 authors at 5 institutions in 3 countries.

Pamela M PegmanSchool of Biotechnology and National Centre for Sensor Research, Dublin City University, Dublin 9, Ireland.
Sinéad M Smith
Brendan N D'Souza
Sinéad T Loughran
Sabine Maier
Bettina Kempkes
Paul A Cahill
Matthew J Simmons
Céline Gélinas
Dermot Walls
Sensor Electronics (United States) · USUrologische Klinik München · DEDublin City University · IEJohnson University · USRutgers, The State University of New Jersey · US

Funding

THE NF KAPPAB SIGNALING PATHWAY, APOPTOSIS AND CANCERR01CA083937 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI GELINAS, CELINE · 2000 to 2011
$2.0M
GRADUATE TRAINING IN CELLULAR AND MOLECULAR BIOLOGYT32GM008360 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI MADURA, KIRAN · 1991 to 2011
$1.1M
NCI NIH HHS CA83937NCI NIH HHS R01 CA083937NIGMS NIH HHS GM08360NIGMS NIH HHS T32 GM008360
6 · The paper itself

Abstract

The human herpesvirus Epstein-Barr virus (EBV) establishes latency and promotes the long-term survival of its host B cell by targeting the molecular machinery controlling cell fate decisions. The cellular antiapoptotic bfl-1 gene confers protection from apoptosis under conditions of growth factor deprivation when expressed ectopically in an EBV-negative Burkitt's lymphoma-derived cell line (B. D'Souza, M. Rowe, and D. Walls, J. Virol. 74:6652-6658, 2000), and the EBV latent membrane protein 1 (LMP1) and its cellular functional homologue CD40 can both drive bfl-1 via an NF-kappaB-dependent enhancer element in the bfl-1 promoter (B. N. D'Souza, L. C. Edelstein, P. M. Pegman, S. M. Smith, S. T. Loughran, A. Clarke, A. Mehl, M. Rowe, C. Gélinas, and D. Walls, J. Virol. 78:1800-1816, 2004). Here we show that the EBV nuclear antigen 2 (EBNA2) also upregulates bfl-1. EBNA2 trans-activation of bfl-1 requires CBF1 (or RBP-J kappa), a nuclear component of the Notch signaling pathway, and there is an essential role for a core consensus CBF1-binding site on the bfl-1 promoter. trans-activation is dependent on the EBNA2-CBF1 interaction, is modulated by other EBV gene products known to interact with the CBF1 corepressor complex, and does not involve activation of NF-kappaB. bfl-1 expression is induced and maintained at high levels by the EBV growth program in a lymphoblastoid cell line, and withdrawal of either EBNA2 or LMP1 does not lead to a reduction in bfl-1 mRNA levels in this context, whereas the simultaneous loss of both EBV proteins results in a major decrease in bfl-1 expression. These findings are relevant to our understanding of EBV persistence, its role in malignant disease, and the B-cell developmental process.

Indexed as

Transcriptional ActivationAntigens, ViralApoptosisBase SequenceBinding SitesB-LymphocytesCells, CulturedEpstein-Barr Virus Nuclear AntigensHerpesvirus 4, HumanHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinMinor Histocompatibility AntigensMolecular Sequence DataPromoter Regions, GeneticProto-Oncogene Proteins c-bcl-2Receptors, NotchAntigens, ViralBCL2-related protein A1EBNA-2 protein, Human herpesvirus 4EBNA-3A antigenEBNA-3B antigenEBNA-3C, epstein-barr virusEBV-associated membrane antigen, Epstein-Barr virusEpstein-Barr Virus Nuclear AntigensImmunoglobulin J Recombination Signal Sequence-Binding ProteinMinor Histocompatibility AntigensProto-Oncogene Proteins c-bcl-2RBPJ protein, humanReceptors, NotchRepressor ProteinsRNA, MessengerViral Matrix ProteinsViral Proteins

Identifiers

PMID16873269
PMCPMC1563820
OpenAlexW2098837692

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.