Evidence map›Paper›PMID 11778704›Full record

ArticleVirus genes2001

The amino acid region 248-382 of the Epstein-Barr virus nuclear protein 2 (EBNA2) is responsible for the EBNA2-induced EBV reactivation.

S Fujiwara, E Liu, K Shimizu

Abstract read
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In one paragraph

Article in Virus genes, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

S FujiwaraDepartment of Immunology and Microbiology, Nihon University School of Medicine, Tokyo, Japan. shige@med.nihon-u.ac.jp
E Liu
K Shimizu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We showed previously that Epstein-Barr virus (EBV) latency is disrupted and the virus-replicative cycle is activated after expression of EBNA2 in the Burkitt's lymphoma-derived Akata cells. Here, an EBNA2 deletion mutant lacking the amino acid residues 248-382, including the region responsible for association with RBP-J kappa, was generated and tested for its ability to activate EBV replication in Akata cells. This mutant was shown clearly deficient in inducing the EBV-replicative cycle, suggesting that association with RBP-J kappa is necessary for the EBV activating function of EBNA2. It is thus likely that EBV activation by EBNA2, seemingly in conflict with its involvement in lymphocyte immortalization, is nevertheless based on the standard mechanism of transactivation by the protein.

Indexed as

Cell LineEpstein-Barr Virus Nuclear AntigensHerpesvirus 4, HumanProtein Structure, TertiaryViral ProteinsVirus ActivationEBNA-2 protein, Human herpesvirus 4Epstein-Barr Virus Nuclear AntigensViral Proteins

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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.