http://purl.uniprot.org/citations/34735924 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/34735924 | http://www.w3.org/2000/01/rdf-schema#comment | "Macrophages play an important role in maintaining tissue homeostasis, from regulating the inflammatory response to pathogens to resolving inflammation and aiding tissue repair. The surfactant protein A (SP-A) receptor SP-R210 (MYO18A) has been shown to affect basal and inflammatory macrophage states. Specifically, disruption of the longer splice isoform SP-R210L/MYO18Aα renders macrophages hyper-inflammatory, although the mechanism by which this occurs is not well understood. We asked whether disruption of the L isoform led to the hyper-inflammatory state via alteration of global genomic responses. RNA sequencing analysis of L isoform-deficient macrophages (SP-R210L(DN)) revealed basal and influenza-induced upregulation of genes associated with inflammatory pathways, such as TLR, RIG-I, NOD, and cytoplasmic DNA signaling, whereas knockout of both SP-R210 isoforms (L and S) only resulted in increased RIG-I and NOD signaling. Chromatin immunoprecipitation sequencing (ChIP-seq) analysis showed increased genome-wide deposition of the pioneer transcription factor PU.1 in SP-R210L(DN) cells, with increased representation around genes relevant to inflammatory pathways. Additional ChIP-seq analysis of histone H3 methylation marks showed decreases in both repressive H3K9me3 and H3K27me3 marks with a commensurate increase in transcriptionally active (H3K4me3) histone marks in the L isoform deficient macrophages. Influenza A virus (IAV) infection, known to stimulate a wide array of anti-viral responses, caused a differential redistribution of PU.1 binding between proximal promoter and distal sites and decoupling from Toll-like receptor regulated gene promoters in SP-R210L(DN) cells. These finding suggest that the inflammatory differences seen in SP-R210L-deficient macrophages are a result of transcriptional differences that are mediated by epigenetic changes brought about by differential expression of the SP-R210 isoforms. This provides an avenue to explore how the signaling pathways downstream of the receptor and the ligands can modulate the macrophage inflammatory response."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.imbio.2021.152150"xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Chen Y."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Song C."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Takahashi Y."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Tang Z."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Webb J."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Carillo M."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Chroneos Z.C."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Umstead T.M."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Kawasawa Y.I."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Dovat S."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/author | "Yau E."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/date | "2021"xsd:gYear |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/name | "Immunobiology"xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/pages | "152150"xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/title | "Genomic and epigenomic adaptation in SP-R210 (Myo18A) isoform-deficient macrophages."xsd:string |
http://purl.uniprot.org/citations/34735924 | http://purl.uniprot.org/core/volume | "226"xsd:string |
http://purl.uniprot.org/citations/34735924 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/34735924 |
http://purl.uniprot.org/citations/34735924 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/34735924 |
http://purl.uniprot.org/uniprot/#_A0A1C7ZN10-mappedCitation-34735924 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/34735924 |
http://purl.uniprot.org/uniprot/#_A0A4Y5WWJ7-mappedCitation-34735924 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/34735924 |
http://purl.uniprot.org/uniprot/#_B2RRE2-mappedCitation-34735924 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/34735924 |
http://purl.uniprot.org/uniprot/#_E9QAX2-mappedCitation-34735924 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/34735924 |