PropertyValue
?:abstract
  • SARS-CoV-2 infection of human airway epithelium activates genetic programs that lead to progressive hyperinflammation in COVID-19 patients. Here we report on the transcriptomic response of airway epithelium to interferons and its suppression by the JAK inhibitors Baricitinib and Ruxolitinib. There is a debate on the regulation of the conventional versus the novel intronic promoter inducing the short ACE2 isoform. Through RNA-seq and ChIP-seq analyses for activating chromatin marks and Polymerase II, we define the interferon-activated intronic regulatory region. Our results also support that the conventional ACE2 promoter is controlled by interferon.
?:creator
?:doi
  • 10.1101/2020.10.04.325415
?:doi
?:journal
  • bioRxiv
?:license
  • cc0
?:pdf_json_files
  • document_parses/pdf_json/04ba6746f480d4ae60d74487de05fb2f0c0381dc.json; document_parses/pdf_json/bd5cd329fcd8b5772cc53158a9eecfd6ef112366.json
?:pmc_json_files
  • document_parses/pmc_json/PMC7553184.xml.json
?:pmcid
?:pmid
?:pmid
  • 33052350.0
?:publication_isRelatedTo_Disease
?:sha_id
?:source
  • BioRxiv; Medline; PMC; WHO
?:title
  • Activation of ACE2 and interferon-stimulated transcriptomes in human airway epithelium is curbed by Janus Kinase inhibitors
?:type
?:year
  • 2020-10-05

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