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Vitenshtein, A.* ; Weisblum, Y.* ; Hauka, S.* ; Halenius, A.* ; Oiknine-Djian, E.* ; Tsukerman, P.* ; Bauman, Y.* ; Bar-On, Y.* ; Stern-Ginossar, N.* ; Enk, J.* ; Ortenberg, R.* ; Tai, J.* ; Markel, G.* ; Blumberg, R.S.* ; Hengel, H.* ; Jonjic, S.* ; Wolf, D.G.* ; Adler, H. ; Kammerer, R.* ; Mandelboim, O.*

CEACAM1-mediated inhibition of virus production.

Cell Rep. 15, 2331-2339 (2016)
Publ. Version/Full Text DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Cells in our body can induce hundreds of antiviral genes following virus sensing, many of which remain largely uncharacterized. CEACAM1 has been previously shown to be induced by various innate systems; however, the reason for such tight integration to innate sensing systems was not apparent. Here, we show that CEACAM1 is induced following detection of HCMV and influenza viruses by their respective DNA and RNA innate sensors, IFI16 and RIG-I. This induction is mediated by IRF3, which bound to an ISRE element present in the human, but not mouse, CEACAM1 promoter. Furthermore, we demonstrate that, upon induction, CEACAM1 suppresses both HCMV and influenza viruses in an SHP2-dependent process and achieves this broad antiviral efficacy by suppressing mTOR-mediated protein biosynthesis. Finally, we show that CEACAM1 also inhibits viral spread in ex vivo human decidua organ culture.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Transcription Factor; Protein; Interferon; Ceacam1; Induction; Adhesion; Innate; Shp-2; Immunity; Antigen
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Journal Cell Reports
Quellenangaben Volume: 15, Issue: 11, Pages: 2331-2339 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place Cambridge
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Research Unit Gene Vector (AGV)