Evidence map›Paper›PMID 10618376›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

IFN consensus sequence binding protein potentiates STAT1-dependent activation of IFNgamma-responsive promoters in macrophages.

C Contursi, I M Wang, L Gabriele, M Gadina, J O'Shea, H C Morse, K Ozato

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Microglia and Brain Macrophages as Drivers of Glioma Progression.International journal of molecular sciences · 2022
    Review
  5. The JAK/STAT signaling pathway: from bench to clinic.Signal transduction and targeted therapy · 2021
    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

7 authors at 2 institutions in 1 country.

C ContursiLaboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
I M Wang
L Gabriele
M Gadina
J O'Shea
H C Morse
K Ozato
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · US

Funding

Lymphomas And Retroviral PathogenesisZIAAI000858 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MORSE, HERBERT · 2009 to 2018
$5.3M
LYMPHOMAS AND RETROVIRAL PATHOGENESISZ01AI000858 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI MORSE, HERBERT C · 2000 to 2008
$2.2M
6 · The paper itself

Abstract

IFNgamma, once called the macrophage-activating factor, stimulates many genes in macrophages, ultimately leading to the elicitation of innate immunity. IFNgamma's functions depend on the activation of STAT1, which stimulates transcription of IFNgamma-inducible genes through the GAS element. The IFN consensus sequence binding protein (icsbgamma or IFN regulatory factor 8), encoding a transcription factor of the IFN regulatory factor family, is one of such IFNgamma-inducible genes in macrophages. We found that macrophages from ICSBP-/- mice were defective in inducing some IFNgamma-responsive genes, even though they were capable of activating STAT1 in response to IFNgamma. Accordingly, IFNgamma activation of luciferase reporters fused to the GAS element was severely impaired in ICSBP-/- macrophages, but transfection of ICSBP resulted in marked stimulation of these reporters. Consistent with its role in activating IFNgamma-responsive promoters, ICSBP stimulated reporter activity in a GAS-specific manner, even in the absence of IFNgamma treatment, and in STAT1 negative cells. Indicative of a mechanism for this stimulation, DNA affinity binding assays revealed that endogenous ICSBP was recruited to a multiprotein complex that bound to GAS. These results suggest that ICSBP, when induced by IFNgamma through STAT1, in turn generates a second wave of transcription from GAS-containing promoters, thereby contributing to the elicitation of IFNgamma's unique activities in immune cells.

Indexed as

AnimalsCell LineDNA-Binding ProteinsGenes, ReporterHumansInterferon-gammaInterferon Regulatory Factor-8Interferon Regulatory FactorsMacrophagesMiceMice, KnockoutPromoter Regions, GeneticRepressor ProteinsReverse Transcriptase Polymerase Chain ReactionSTAT1 Transcription FactorTrans-ActivatorsDNA-Binding ProteinsInterferon-gammaInterferon Regulatory Factor-8Interferon Regulatory FactorsRepressor ProteinsSTAT1 protein, humanStat1 protein, mouseSTAT1 Transcription FactorTrans-Activators

Identifiers

PMID10618376
PMCPMC26621
OpenAlexW2034779553

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.