Evidence map›Paper›PMID 1406670›Full record

ArticleMolecular and cellular biology1992

The EBNA2-related resistance towards alpha interferon (IFN-alpha) in Burkitt's lymphoma cells effects induction of IFN-induced genes but not the activation of transcription factor ISGF-3.

K Kanda, T Decker, P Aman, M Wahlström, A von Gabain, B Kallin

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

25 citing papers in PubMed, 72 citations in OpenAlex.

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  12. Regulation of Sp100A subnuclear localization and transcriptional function by EBNA-LP and interferon.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2008
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  16. Human cytomegalovirus UL83-coded pp65 virion protein inhibits antiviral gene expression in infected cells.Proceedings of the National Academy of Sciences of the United States of America · 2003
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

K KandaDepartment of Bacteriology, Karolinska Institute, Stockholm, Sweden.
T Decker
P Aman
M Wahlström
A von Gabain
B Kallin
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transfection of a plasmid encoding the Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA2) gene confers resistance to the antiproliferative effect of alpha interferon (IFN-alpha) in EBV-negative U968 cells (P. Aman and A. von Gabain, EMBO J. 9:147-152, 1990). We studied the expression of IFN-stimulated genes (ISGs) in two pairs of Burkitt's lymphoma cell lines, differing in the expression of the putative immortalizing gene of EBV, EBNA2. In EBNA2-expressing cells, the induction of four ISGs by IFN-alpha was strongly reduced or, in some cases, abolished. Chloramphenicol acetyltransferase reporter gene constructs containing different IFN-stimulated response elements were transfected into EBNA2-negative and EBNA2-positive cells. Induction of chloramphenicol acetyltransferase activity by IFN was impaired in EBNA2-positive cells. Also, a reporter gene construct driven by an IFN-gamma-sensitive promoter element was affected. However, as revealed by gel shift assays, EBNA2-positive and EBNA2-negative cells exhibited a nearly identical pattern of IFN-stimulated response element-binding proteins. Most important, activation of the factor ISGF-3, which previously has been shown to be required and sufficient for transcriptional activation of IFN-induced genes, was not inhibited in IFN-resistant cells expressing EBNA2. The mechanism of the EBNA2-related IFN resistance seems to be distinct both from the resistance mediated by hepatitis virus and adenovirus gene products and from the IFN resistance in Daudi cell variants. In these three cases, the transcriptional block of IFN-induced genes is due to inhibition of ISGF-3 activation and binding. Our data suggest that the EBNA2-related IFN resistance in Burkitt's lymphoma cells acts downstream of the activation of ISGF-3.

Indexed as

Gene Expression RegulationAntigens, ViralBlotting, NorthernBurkitt LymphomaDNA-Binding ProteinsDrug ResistanceEpstein-Barr Virus Nuclear AntigensInterferon-alphaInterferon-Stimulated Gene Factor 3Transcription FactorsTranscription, GeneticTumor Cells, CulturedAntigens, ViralDNA-Binding ProteinsEpstein-Barr Virus Nuclear AntigensInterferon-alphaInterferon-Stimulated Gene Factor 3Transcription Factors

Identifiers

PMID1406670
PMCPMC360425
OpenAlexW1887290302

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.