Evidence map›Paper›PMID 24065129›Full record

ArticleThe EMBO journal2013

IFNβ-dependent increases in STAT1, STAT2, and IRF9 mediate resistance to viruses and DNA damage.

HyeonJoo Cheon, Elise G Holvey-Bates, John W Schoggins, Samuel Forster, Paul Hertzog, Naoko Imanaka, Charles M Rice, Mark W Jackson, Damian J Junk, George R Stark

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 245 papers.

0numbers the graph read from it
0cells of the map it votes in
245citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

245 citing papers in PubMed, 331 citations in OpenAlex.

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  14. L-lactic acid enhances type I interferon immune response and inhibits virus infection by promoting IRF9 L-lactylation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  19. Identification of AMOTL2 as an antiviral factor that enhances the human type I interferon response against Zika virus.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Review

185 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

10 authors at 4 institutions in 2 countries.

HyeonJoo CheonDepartment of Molecular Genetics, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Elise G Holvey-Bates
John W Schoggins
Samuel Forster
Paul Hertzog
Naoko Imanaka
Charles M Rice
Mark W Jackson
Damian J Junk
George R Stark
Cleveland Clinic Lerner College of Medicine · USRockefeller University · USCase Western Reserve University · USMonash Institute of Medical Research · AU

Funding

TELOMERASE INACTIVATION BY RNASE L SIGNALS CELL DEATHP01CA062220 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI STARK, GEORGE ROBERT · 1994 to 2020
$35.6M
RESEARCH ONCOLOGY TRAINING GRANTT32CA059366 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI JACKSON, MARK W. · 1993 to 2025
$5.5M
Type I interferon-stimulated genes and the antiviral immune responseR01AI091707 · NIAID · ROCKEFELLER UNIVERSITY · PI RICE, CHARLES M · 2011 to 2020
$5.5M
Interactions between type I and III interferon during resolution of HCV infectionK01DK095031 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI SCHOGGINS, JOHN W. · 2012 to 2016
$629k
NCI NIH HHS P01 CA062220NCI NIH HHS T32 CA059366NIAID NIH HHS R01 AI091707NIDDK NIH HHS K01 DK095031
6 · The paper itself

Abstract

A single high dose of interferon-β (IFNβ) activates powerful cellular responses, in which many anti-viral, pro-apoptotic, and anti-proliferative proteins are highly expressed. Since some of these proteins are deleterious, cells downregulate this initial response rapidly. However, the expression of many anti-viral proteins that do no harm is sustained, prolonging a substantial part of the initial anti-viral response for days and also providing resistance to DNA damage. While the transcription factor ISGF3 (IRF9 and tyrosine-phosphorylated STATs 1 and 2) drives the first rapid response phase, the related factor un-phosphorylated ISGF3 (U-ISGF3), formed by IFNβ-induced high levels of IRF9 and STATs 1 and 2 without tyrosine phosphorylation, drives the second prolonged response. The U-ISGF3-induced anti-viral genes that show prolonged expression are driven by distinct IFN stimulated response elements (ISREs). Continuous exposure of cells to a low level of IFNβ, often seen in cancers, leads to steady-state increased expression of only the U-ISGF3-dependent proteins, with no sustained increase in other IFNβ-induced proteins, and to constitutive resistance to DNA damage.

Indexed as

Disease ResistanceDNA DamageAnimalsAntiviral AgentsCells, CulturedChlorocebus aethiopsGene Expression RegulationHumansInterferon-betaInterferon-Stimulated Gene Factor 3, gamma SubunitSTAT1 Transcription FactorSTAT2 Transcription FactorTumor EscapeVero CellsVirus DiseasesVirusesAntiviral AgentsInterferon-betaInterferon-Stimulated Gene Factor 3, gamma SubunitIRF9 protein, humanSTAT1 protein, humanSTAT1 Transcription FactorSTAT2 protein, humanSTAT2 Transcription Factor

Identifiers

PMID24065129
PMCPMC3801437
OpenAlexW2113174452

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.