ArticleThe Journal of biological chemistry2011
Chromatin dynamics of gene activation and repression in response to interferon alpha (IFN(alpha)) reveal new roles for phosphorylated and unphosphorylated forms of the transcription factor STAT2.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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.
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.
Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- The HIV-1 restriction factor RPRD2 does not inhibit transcription of HIV-1 or endogenous retroelements.bioRxiv : the preprint server for biology · 2026Article
- Regulatory Roles of SWI/SNF Chromatin Remodeling Complexes in Immune Response and Inflammatory Diseases.Clinical reviews in allergy & immunology · 2024Review
- Functional Involvement of Signal Transducers and Activators of Transcription in the Pathogenesis of Influenza A Virus.International journal of molecular sciences · 2024Review
- Review
- Epigenetic signals that direct cell type-specific interferon beta response in mouse cells.Life science alliance · 2023Article
- How cancer cells make and respond to interferon-I.Trends in cancer · 2023Review
- Regulation of macrophage IFNγ-stimulated gene expression by the transcriptional coregulator CITED1.Journal of cell science · 2023Article
- Exposing the Two Contrasting Faces of STAT2 in Inflammation.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Review
- BRD9 regulates interferon-stimulated genes during macrophage activation via cooperation with BET protein BRD4.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Interferon stimulated binding of ISRE is cell type specific and is predicted by homeostatic chromatin state.Cytokine: X · 2021Article
- Review
- Targeted Stat2 deletion in conventional dendritic cells impairs CTL responses but does not affect antibody production.Oncoimmunology · 2020Article
- Article
- Interferon Response in Hepatitis C Virus-Infected Hepatocytes: Issues to Consider in the Era of Direct-Acting Antivirals.International journal of molecular sciences · 2020Review
- Interferon signaling during Hepatitis B Virus (HBV) infection and HBV-associated hepatocellular carcinoma.Cytokine · 2019Review
- A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.Nature communications · 2019Article
- Differential roles of STAT1 and STAT2 in the sensitivity of JAK2V617F- vs. BCR-ABL-positive cells to interferon alpha.Journal of hematology & oncology · 2019Article
- Implications of STAT3 and STAT5 signaling on gene regulation and chromatin remodeling in hematopoietic cancer.Leukemia · 2018Review
- Molecular cross-talk of IL-6 in tumors and new progress in combined therapy.Thoracic cancer · 2018Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal transducer and activator of transcription 2 (STAT2), the critical component of type I interferons signaling, is a prototype latent cytoplasmic signal-dependent transcription factor. Activated tyrosine-phosphorylated STAT2 associates with STAT1 and IRF9 to bind the ISRE elements in the promoters of a subset of IFN-inducible genes (ISGs). In addition to activate hundreds of ISGs, IFNα also represses numerous target genes but the mechanistic basis for this dual effect and transcriptional repression is largely unknown. We investigated by ChIP-chip the binding dynamics of STAT2 and "active" phospho(P)-STAT2 on 113 putative IFNα direct target promoters before and after IFNα induction in Huh7 cells and primary human hepatocytes (PHH). STAT2 is already bound to 62% of our target promoters, including most "classical" ISGs, before IFNα treatment. 31% of STAT2 basally bound promoters also show P-STAT2 positivity. By correlating in vivo promoter occupancy with gene expression and changes in histone methylation marks we found that: 1) STAT2 plays a role in regulating ISGs expression, independently from its phosphorylation; 2) P-STAT2 is involved in ISGs repression; 3) "activated" ISGs are marked by H3K4me1 and H3K4me3 before IFNα; 4) "repressed" genes are marked by H3K27me3 and histone methylation plays a dominant role in driving IFNα-mediated ISGs repression.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.