ArticleCytokine: X2021
Interferon stimulated binding of ISRE is cell type specific and is predicted by homeostatic chromatin state.
Article in Cytokine: X, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Context matters: Conflicting roles of interferon-γ signaling in CNS diseases.Current opinion in neurobiology · 2026Review
- Fish TOLLIP manipulates ATG5 for autophagic degradation of STING to attenuate antiviral interferon responses.PLoS pathogens · 2025Article
- MITD1 is a brain-specific interferon-inducible factor that inhibits flavivirus replication.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cell-type-specific requirement for TYK2 in murine immune cells under steady state and challenged conditions.Cellular and molecular life sciences : CMLS · 2025Article
- Identification of interferon-stimulated response elements (ISREs) in canines.BMC veterinary research · 2025Article
- IFNα Subtypes in HIV Infection and Immunity.Viruses · 2024Review
- Toward a comprehensive catalog of regulatory elements.Human genetics · 2023Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The type I interferon (IFN) signaling pathway involves binding of the transcription factor ISGF3 to IFN-stimulated response elements, ISREs. Gene expression under IFN stimulation is known to vary across cell types, but variation in ISGF3 binding to ISRE across cell types has not been characterized. We examined ISRE binding patterns under IFN stimulation across six cell types using existing ChIPseq datasets. We find that ISRE binding is largely cell specific for ISREs distal to transcription start sites (TSS) and largely conserved across cell types for ISREs proximal to TSS. We show that bound ISRE distal to TSS associate with differential expression of ISGs, although at weaker levels than bound ISRE proximal to TSS. Using existing ATACseq and ChIPseq datasets, we show that the chromatin state of ISRE at homeostasis is cell type specific and is predictive of cell specific, ISRE binding under IFN stimulation. Our results support a model in which the chromatin state of ISRE in enhancer elements is modulated in a cell type specific manner at homeostasis, leading to cell type specific differences in ISRE binding patterns under IFN stimulation.
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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.