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10.1084/jem.20210039

http://scihub22266oqcxt.onion/10.1084/jem.20210039
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34297037!8313408!34297037
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suck abstract from ncbi


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pmid34297037      J+Exp+Med 2021 ; 218 (9): ä
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  • Epigenetic and transcriptional control of interferon-beta #MMPMID34297037
  • Daman AW; Josefowicz SZ
  • J Exp Med 2021[Sep]; 218 (9): ä PMID34297037show ga
  • The three classes of interferons (IFNs) share the ability to inhibit viral replication, activating cell transcriptional programs that regulate both innate and adaptive responses to viral and intracellular bacterial challenge. Due to their unique potency in regulating viral replication, and their association with numerous autoimmune diseases, the tightly orchestrated transcriptional regulation of IFNs has long been a subject of intense investigation. The protective role of early robust IFN responses in the context of infection with SARS-CoV-2 has further underscored the relevance of these pathways. In this viewpoint, rather than focusing on the downstream effects of IFN signaling (which have been extensively reviewed elsewhere), we will summarize the historical and current understanding of the stepwise assembly and function of factors that regulate IFNbeta enhancer activity (the "enhanceosome") and highlight opportunities for deeper understanding of the transcriptional control of the ifnb gene.
  • |*Epigenesis, Genetic[MESH]
  • |*Gene Expression Regulation[MESH]
  • |CCAAT-Enhancer-Binding Proteins/genetics/metabolism[MESH]
  • |DNA Methylation[MESH]
  • |Enhancer Elements, Genetic[MESH]
  • |Host-Pathogen Interactions/genetics/*physiology[MESH]
  • |Humans[MESH]
  • |Influenza A Virus, H5N1 Subtype/pathogenicity[MESH]
  • |Interferon-beta/*genetics/metabolism[MESH]
  • |Promoter Regions, Genetic[MESH]
  • |SARS-CoV-2/pathogenicity[MESH]
  • |Transcription, Genetic[MESH]


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