prikaz prve stranice dokumenta The herpesviral antagonist m152 reveals differential activation of STING‐dependent IRF and NF‐κB signaling and STING's dual role during MCMV infection
  Download
PDF 7.61 MB
Scientific paper - Original scientific paper
The herpesviral antagonist m152 reveals differential activation of STING‐dependent IRF and NF‐κB signaling and STING's dual role during MCMV infection
The EMBO Journal, 38 (2019), 5; 100983. https://doi.org/10.15252/embj.2018100983
Stempel, Markus; Chan, Baca; Juranić Lisnić, Vanda; Krmpotić, Astrid; Hartung, Josephine; Paludan, Søren R; Füllbrunn, Nadia; Lemmermann, Niels AW; Brinkmann, Melanie M.

Cite this document

Stempel, M., Chan, B., Juranić Lisnić, V., Krmpotić, A., Hartung, J., Paludan, S. R. ... Brinkmann, M. M. (2019). The herpesviral antagonist m152 reveals differential activation of STING‐dependent IRF and NF‐κB signaling and STING's dual role during MCMV infection. The EMBO Journal, 38. (5). doi: 10.15252/embj.2018100983

Stempel, Markus, et al. "The herpesviral antagonist m152 reveals differential activation of STING‐dependent IRF and NF‐κB signaling and STING's dual role during MCMV infection." The EMBO Journal, vol. 38, no. 5, 2019. https://doi.org/10.15252/embj.2018100983

Stempel, Markus, Baca Chan, Vanda Juranić Lisnić, Astrid Krmpotić, Josephine Hartung, Søren R Paludan, Nadia Füllbrunn, Niels AW Lemmermann and Melanie M. Brinkmann. "The herpesviral antagonist m152 reveals differential activation of STING‐dependent IRF and NF‐κB signaling and STING's dual role during MCMV infection." The EMBO Journal 38, no. 5 (2019). https://doi.org/10.15252/embj.2018100983

Stempel, M., et al. (2019) 'The herpesviral antagonist m152 reveals differential activation of STING‐dependent IRF and NF‐κB signaling and STING's dual role during MCMV infection', The EMBO Journal, 38(5). doi: 10.15252/embj.2018100983

Stempel M, Chan B, Juranić Lisnić V, Krmpotić A, Hartung J, Paludan SR, and sur.. The herpesviral antagonist m152 reveals differential activation of STING‐dependent IRF and NF‐κB signaling and STING's dual role during MCMV infection. The EMBO Journal [Internet]. 2019 January 29 [cited 2024 November 16];38(5). doi: 10.15252/embj.2018100983

M. Stempel, et al., "The herpesviral antagonist m152 reveals differential activation of STING‐dependent IRF and NF‐κB signaling and STING's dual role during MCMV infection", The EMBO Journal, vol. 38, no. 5, January 2019. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:499363. [Accessed: 16 November 2024]

Please login to the repository to save this object to your list.
Metadata
Title (english)The herpesviral antagonist m152 reveals differential activation of STING‐dependent IRF and NF‐κB signaling and STING's dual role during MCMV infection
AuthorMarkus Stempel
AuthorBaca Chan
AuthorVanda Juranić Lisnić
AuthorAstrid Krmpotić
AuthorJosephine Hartung
AuthorSøren R Paludan
AuthorNadia Füllbrunn
AuthorNiels AW Lemmermann
AuthorMelanie M. Brinkmann
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Center for Proteomics)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
Cytomegaloviruses (CMVs) are master manipulators of the host immune response. Here, we reveal that the murine CMV (MCMV) protein m152 specifically targets the type I interferon (IFN) response by binding to stimulator of interferon genes (STING), thereby delaying its trafficking to the Golgi compartment from where STING initiates type I IFN signaling. Infection with an MCMV lacking m152 induced elevated type I IFN responses and this leads to reduced viral transcript levels both in vitro and in vivo This effect is ameliorated in the absence of STING Interestingly, while m152 inhibits STING-mediated IRF signaling, it did not affect STING-mediated NF-κB signaling. Analysis of how m152 targets STING translocation reveals that STING activates NF-κB signaling already from the ER prior to its trafficking to the Golgi. Strikingly, this response is important to promote early MCMV replication. Our results show that MCMV has evolved a mechanism to specifically antagonize the STING-mediated antiviral IFN response, while preserving its pro-viral NF-κB response, providing an advantage in the establishment of an infection.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionAccepted version
Journal titleThe EMBO Journal
Numberingvol. 38, no. 5, 100983
p-ISSN0261-4189
e-ISSN1460-2075
DOIhttps://doi.org/10.15252/embj.2018100983
URN:NBNurn:nbn:hr:184:499363
Online first2019-01-29
ProjectNumber: KK.011.1.01.0006
Title (croatian): Jačanje kapaciteta CerVirVac-a za istraživanja u virusnoj imunologiji i vakcinologiji
Leader: Stipan Jonjić
Jurisdiction: eu
ProjectNumber: N/A
Title (croatian): Centar izvrsnosti za virusnu imunologiju i cjepiva
Title (english): Centre of Excellence for Research in Viral Immunology and the Development of New Vaccines
Acronym: CERVirVac
Leader: Stipan Jonjić
Jurisdiction: Croatia
Funding stream: ZCI
Document URLhttp://emboj.embopress.org/lookup/doi/10.15252/embj.2018100983
Type of resourceText
Access conditionsOpen access
Terms of useLicence Attribution 4.0 International (CC BY 4.0) icon
Created on2019-02-01 10:12:27