prikaz prve stranice dokumenta Differential Susceptibility of RAE-1 Isoforms to Mouse Cytomegalovirus
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Scientific paper - Original scientific paper
Differential Susceptibility of RAE-1 Isoforms to Mouse Cytomegalovirus
Journal of Virology, 83 (2009), 16; 8198-8207. https://doi.org/10.1128/JVI.02549-08
Arapović, Jurica; Lenac, Tihana; Antulov, Ronald; Polić, Bojan; Ruzsics, Z.; Carayannopoulos, L. N.; Koszinowski, U. H.; Krmpotić, Astrid; Jonjić, Stipan

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Arapović, J., Lenac, T., Antulov, R., Polić, B., Ruzsics, Z., Carayannopoulos, L. N. ... Jonjić, S. (2009). Differential Susceptibility of RAE-1 Isoforms to Mouse Cytomegalovirus. Journal of Virology, 83. (16), 8198-8207. doi: 10.1128/JVI.02549-08

Arapović, Jurica, et al. "Differential Susceptibility of RAE-1 Isoforms to Mouse Cytomegalovirus." Journal of Virology, vol. 83, no. 16, 2009, pp. 8198-8207. https://doi.org/10.1128/JVI.02549-08

Arapović, Jurica, Tihana Lenac, Ronald Antulov, Bojan Polić, Z. Ruzsics, L. N. Carayannopoulos, U. H. Koszinowski, Astrid Krmpotić and Stipan Jonjić. "Differential Susceptibility of RAE-1 Isoforms to Mouse Cytomegalovirus." Journal of Virology 83, no. 16 (2009): 8198-8207. https://doi.org/10.1128/JVI.02549-08

Arapović, J., et al. (2009) 'Differential Susceptibility of RAE-1 Isoforms to Mouse Cytomegalovirus', Journal of Virology, 83(16), pp. 8198-8207. doi: 10.1128/JVI.02549-08

Arapović J, Lenac T, Antulov R, Polić B, Ruzsics Z, Carayannopoulos LN, and sur.. Differential Susceptibility of RAE-1 Isoforms to Mouse Cytomegalovirus. Journal of Virology [Internet]. 2009 June 03 [cited 2024 May 13];83(16):8198-8207. doi: 10.1128/JVI.02549-08

J. Arapović, et al., "Differential Susceptibility of RAE-1 Isoforms to Mouse Cytomegalovirus", Journal of Virology, vol. 83, no. 16, pp. 8198-8207, June 2009. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:478936. [Accessed: 13 May 2024]

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Metadata
Title (english)Differential Susceptibility of RAE-1 Isoforms to Mouse Cytomegalovirus
AuthorJurica Arapović
AuthorTihana Lenac
AuthorRonald Antulov
AuthorBojan Polić
AuthorZ. Ruzsics
AuthorL. N. Carayannopoulos
AuthorU. H. Koszinowski
AuthorAstrid Krmpotić
AuthorStipan Jonjić
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Histology and Embryology)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
The NKG2D receptor is one of the most potent activating natural killer cell receptors involved in antiviral responses. The mouse NKG2D ligands MULT-1, RAE-1, and H60 are regulated by murine cytomegalovirus (MCMV) proteins m145, m152, and m155, respectively. In addition, the m138 protein interferes with the expression of both MULT-1 and H60. We show here that one of five RAE-1 isoforms, RAE-1, is resistant to downregulation by MCMV and that this escape has functional importance in vivo. Although m152 retained newly synthesized RAE-1 and RAE-1 in the endoplasmic reticulum, no viral regulator was able to affect the mature RAE-1 form which remains expressed on the surfaces of infected cells. This differential susceptibility to downregulation by MCMV is not a consequence of faster maturation of RAE-1 compared to RAE-1 but rather an intrinsic property of the mature surface-resident protein. This difference can be attributed to the absence of a PLWY motif from RAE-1. Altogether, these findings provide evidence for a novel mechanism of host escape from viral immunoevasion of NKG2D-dependent control.
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionPublished version
Journal titleJournal of Virology
Numberingvol. 83, no. 16, pp. 8198-8207
p-ISSN0022-538X
DOIhttps://doi.org/10.1128/JVI.02549-08
URN:NBNurn:nbn:hr:184:478936
Publication2009-06-03
Publication2009-08-15
Document URLhttp://jvi.asm.org/cgi/doi/10.1128/JVI.02549-08
Type of resourceText
Access conditionsOpen access
Terms of useLicence Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) icon
Created on2018-11-08 22:28:08