Please use this identifier to cite or link to this item: https://doi.org/10.1042/BSR20181059
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dc.titleOverexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10
dc.contributor.authorAboagye, James Odame
dc.contributor.authorYew, Chow Wenn
dc.contributor.authorNg, Oi-Wing
dc.contributor.authorMonteil, Vanessa M
dc.contributor.authorMirazimi, Ali
dc.contributor.authorTan, Yee-Joo
dc.date.accessioned2022-04-20T07:12:58Z
dc.date.available2022-04-20T07:12:58Z
dc.date.issued2018-10-31
dc.identifier.citationAboagye, James Odame, Yew, Chow Wenn, Ng, Oi-Wing, Monteil, Vanessa M, Mirazimi, Ali, Tan, Yee-Joo (2018-10-31). Overexpression of the nucleocapsid protein of Middle East respiratory syndrome coronavirus up-regulates CXCL10. BIOSCIENCE REPORTS 38 (5). ScholarBank@NUS Repository. https://doi.org/10.1042/BSR20181059
dc.identifier.issn01448463
dc.identifier.issn15734935
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/219376
dc.description.abstractMiddle 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.language.isoen
dc.publisherPORTLAND PRESS LTD
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectBiochemistry & Molecular Biology
dc.subjectCell Biology
dc.subjectDENDRITIC CELLS
dc.subjectPATHOGENESIS
dc.subjectREPLICATION
dc.subjectINDUCTION
dc.subjectMACROPHAGES
dc.subjectCYTOKINES
dc.subjectDISEASE
dc.typeArticle
dc.date.updated2022-04-20T04:38:50Z
dc.contributor.departmentDEPT OF BIOCHEMISTRY
dc.contributor.departmentDEPT OF MICROBIOLOGY & IMMUNOLOGY
dc.description.doi10.1042/BSR20181059
dc.description.sourcetitleBIOSCIENCE REPORTS
dc.description.volume38
dc.description.issue5
dc.published.statePublished
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