Evidence map›Paper›PMID 19929594›Full record

ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2009

Roles of IKK-beta, IRF1, and p65 in the activation of chemokine genes by interferon-gamma.

David B Shultz, M R Sandhya Rani, John D Fuller, Richard M Ransohoff, George R Stark

Open access · greenAbstract read
In one paragraph

Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

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  12. SNX8 mediates IFNγ-triggered noncanonical signaling pathway and host defense againstProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
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  18. EGFR activation suppresses respiratory virus-induced IRF1-dependent CXCL10 production.American journal of physiology. Lung cellular and molecular physiology · 2014
    Article
  19. A role for human brain pericytes in neuroinflammation.Journal of neuroinflammation · 2014
    Article
  20. Article
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

5 authors at 2 institutions in 1 country.

David B ShultzDepartment of Molecular Genetics, Cleveland Clinic, Cleveland, Ohio 44195, USA.
M R Sandhya Rani
John D Fuller
Richard M Ransohoff
George R Stark
Cleveland Clinic · USCase Western Reserve University · US

Funding

TELOMERASE INACTIVATION BY RNASE L SIGNALS CELL DEATHP01CA062220 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI LI, XIAOXIA, STARK, GEORGE ROBERT · 1994 to 2020
$35.6M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
NCI NIH HHS P01 CA 062220NIGMS NIH HHS T32 GM007250NIGMS NIH HHS T32 GM07250
6 · The paper itself

Abstract

Activation of chemokine genes in response to interferon (IFN)-gamma or NF-kappaB is an important aspect of inflammation. Using the chemokine gene ip-10 in mouse embryonic fibroblast cells as an example, we show that the response to IFN-gamma is long lasting but secondary: initial STAT1 activation drives IRF1 synthesis, and IRF1 then binds to IFN-stimulated regulatory elements (ISREs) in the ip-10 promoter. The promoters of most IKK-beta-dependent IFN-stimulated genes (ISGs) also contain ISREs. In response to IFN-gamma, inhibitor of NF-kappaB (IkappaB) kinase beta (IKK-beta) is required to activate both newly synthesized IRF1 and the p65 subunit of NF-kappaB, which contributes to ip-10 expression by binding to kappaB sites in the ip-10 promoter, with little or no activation of classical NF-kappaB. In contrast to IFN-gamma, IL-1beta induces ip-10 expression rapidly but transiently, by activating classical NF-kappaB and increasing the synthesis of IRF1. Together, IL-1beta and IFN-gamma induce ip-10 synergistically. IFN-gamma does not affect the transient activation of classical NF-kappaB by IL-1beta and synergistic induction of ip-10 expression by IFN-gamma and IL-1beta occurs even after the activation of classical NF-kappaB has returned to basal levels. Therefore, IKK-beta has a novel role in IFN-gamma-dependent activation of chemokine gene expression through its activation of IRF1 and p65.

Indexed as

Transcriptional ActivationAnimalsChemokine CXCL10ChemokinesI-kappa B KinaseInterferon-gammaInterferon Regulatory Factor-1Interferon Regulatory FactorsInterleukin-1betaMicePromoter Regions, GeneticSignal TransductionTranscription Factor RelAChemokine CXCL10ChemokinesI-kappa B KinaseInterferon-gammaInterferon Regulatory Factor-1Interferon Regulatory FactorsInterleukin-1betaRela protein, mouseTranscription Factor RelA

Identifiers

PMID19929594
PMCPMC2956658
OpenAlexW1966028027

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.