Evidence map›Paper›PMID 10490661›Full record

ArticleMolecular and cellular biology1999

Transcriptional repression of Stat6-dependent interleukin-4-induced genes by BCL-6: specific regulation of iepsilon transcription and immunoglobulin E switching.

M B Harris, C C Chang, M T Berton, N N Danial, J Zhang, D Kuehner, B H Ye, M Kvatyuk, P P Pandolfi, G Cattoretti and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.

  1. Pooled it
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  17. Replication study of susceptibility variants associated with allergic rhinitis and allergy in Han Chinese.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2020
    Article
  18. IgE Glycosylation in Health and Disease.Current topics in microbiology and immunology · 2019
    Review
  19. Article
  20. Article

5 more citing papers are in PubMed but not listed here.

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

12 authors at 5 institutions in 3 countries.

M B HarrisIntegrated Program in Cellular, Molecular and Biophysical Sciences, Columbia University College of Physicians and Surgeons, New York, New York.
C C Chang
M T Berton
N N Danial
J Zhang
D Kuehner
B H Ye
M Kvatyuk
P P Pandolfi
G Cattoretti
R Dalla-Favera
P B Rothman
Columbia University · USColumbia College · CAMemorial Sloan Kettering Cancer Center · USRoyal College of Physicians · GBThe University of Texas Health Science Center at San Antonio · US

Funding

SDF1 IN MESENCHYMAL ALTERATIONS OF IMMUNE INJURYP01AI039675 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CHESS, LEONARD · 1996 to 1999
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NIAID NIH HHS P01AI39675
6 · The paper itself

Abstract

The BCL-6 proto-oncogene encodes a POZ/zinc-finger transcription factor that is expressed in B cells and a subset of CD4(+) T cells within germinal centers. Recent evidence suggests that BCL-6 can act as a sequence-specific repressor of transcription, but the target genes for this activity have not yet been identified. The binding site for BCL-6 shares striking homology to the sites that are the target sequence for the interleukin-4 (IL-4)-induced Stat6 (signal transducers and activators of transcription) signaling molecule. Electrophoretic mobility shift assays demonstrate that BCL-6 can bind, with different affinities, to several DNA elements recognized by Stat6. Expression of BCL-6 can repress the IL-4-dependent induction of immunoglobulin (Ig) germ line epsilon transcripts, but does not repress the IL-4 induction of CD23 transcripts. Consistent with the role of BCL-6 in modulating transcription from the germ line epsilon promoter, BCL-6(-/-) mice display an increased ability to class switch to IgE in response to IL-4 in vitro. These animals also exhibit a multiorgan inflammatory disease characterized by the presence of a large number of IgE(+) B cells. The apparent dysregulation of IgE production is abolished in BCL-6(-/-) Stat6(-/-) mice, indicating that BCL-6 regulation of Ig class switching is dependent upon Stat6 signaling. Thus, BCL-6 can modulate the transcription of selective Stat6-dependent IL-4 responses, including IgE class switching in B cells.

Indexed as

Immunoglobulin Class SwitchingAnimalsBinding SitesB-LymphocytesDNA-Binding ProteinsGene Expression RegulationGerm CellsImmunoglobulin EInterleukin-4MiceMice, KnockoutProtein BindingProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-6Signal TransductionSTAT6 Transcription FactorDNA-Binding ProteinsImmunoglobulin EInterleukin-4Proto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-6Stat6 protein, mouseSTAT6 Transcription FactorTrans-ActivatorsTranscription Factors

Identifiers

PMID10490661
PMCPMC84719
OpenAlexW2099044445

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.