@prefix : <http://semanticscholar.org/cv-research/> .
@prefix dc: <http://purl.org/dc/terms/> .
@prefix fhir_link: <http://hl7.org/fhir/link/> .
@prefix ncit: <http://ncicb.nci.nih.gov/xml/owl/EVS/Thesaurus.owl#> .
@prefix rdf: <http://www.w3.org/1999/02/22-rdf-syntax-ns#> .
@prefix rdfs: <http://www.w3.org/2000/01/rdf-schema#> .
@prefix sso: <http://semanticscholar.org/cv-research/> .
@prefix whocv: <http://semanticscholar.org/cv-research/WHO#> .
@prefix xml: <http://www.w3.org/XML/1998/namespace> .
@prefix xsd: <http://www.w3.org/2001/XMLSchema#> .

<http://fhircat.org/cord-19/metadata/7b830ff35cb63eec2889a5d21a0d49d1f8c687c3> dc:abstract "Middle East respiratory syndrome coronavirus (MERS-CoV) causes respiratory diseases in humans and has a high mortality rate. During infection, MERS-CoV regulates several host cellular processes including antiviral response genes. In order to determine if the nucleocapsid protein of MERS-CoV (MERS-N) plays a role in viral–host interactions, a murine monoclonal antibody was generated so as to allow detection of the protein in infected cells as well as in overexpression system. Then, MERS-N was stably overexpressed in A549 cells, and a PCR array containing 84 genes was used to screen for genes transcriptionally regulated by it. Several up-regulated antiviral genes, namely TNF, IL6, IL8, and CXCL10, were selected for independent validation in transiently transfected 293FT cells. Out of these, the overexpression of MERS-N was found to up-regulate CXCL10 at both transcriptional and translational levels. Interestingly, CXCL10 has been reported to be up-regulated in MERS-CoV infected airway epithelial cells and lung fibroblast cells, as well as monocyte-derived macrophages and dendritic cells. High secretions and persistent increase of CXCL10 in MERS-CoV patients have been also associated with severity of disease. To our knowledge, this is the first report showing that the MERS-N protein is one of the contributing factors for CXCL10 up-regulation during infection. In addition, our results showed that a fragment consisting of residues 196–413 in MERS-N is sufficient to up-regulate CXCL10, while the N-terminal domain and serine-arginine (SR)-rich motif of MERS-N do not play a role in this up-regulation." ;
    dc:creator "['Aboagye, James\\xa0Odame', 'Yew, Chow\\xa0Wenn', 'Ng, Oi-Wing', 'Monteil, Vanessa\\xa0M.', 'Mirazimi, Ali', 'Tan, Yee-Joo']" ;
    dc:identifier <http://dx.doi.org/10.1042/BSR20181059>,
        <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6200698>,
        <https://www.ncbi.nlm.nih.gov/pubmed/30242057> ;
    dc:issued "2018-01-01"^^xsd:date ;
    dc:license "CC BY" ;
    dc:title "Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10" ;
    sso:has_full_text "False" ;
    sso:journal "Biosci Rep" ;
    sso:sha "7b830ff35cb63eec2889a5d21a0d49d1f8c687c3" ;
    sso:source_x "PMC" .

