Pregled bibliografske jedinice broj: 134481
A viral protein reveals a biological role for STAT2 in IFN-gamma receptor signaling
A viral protein reveals a biological role for STAT2 in IFN-gamma receptor signaling // Final programme and abstract book ; 9th International Cytomegalovirus Workshop and 1st International Betaherpesvirus Workshop / Bruggeman, Cathrien ; Vink, Kees ; Claus-Hahn, Fia ; (ur.).
Maastricht, 2003. (poster, nije recenziran, sažetak, znanstveni)
CROSBI ID: 134481 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
A viral protein reveals a biological role for STAT2 in IFN-gamma receptor signaling
Autori
Zimmermann, Albert ; Wilborn, Manuel ; Wagner, Marcus ; Ziade, Toufic ; Bubic, Ivan ; Trilling, Mirko ; Jonjić, Stipan ; Koszinowski, Ulrich ; Hengel, Hartmut ;
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
Final programme and abstract book ; 9th International Cytomegalovirus Workshop and 1st International Betaherpesvirus Workshop
/ Bruggeman, Cathrien ; Vink, Kees ; Claus-Hahn, Fia ; - Maastricht, 2003
Skup
9th International Cytomegalovirus Workshop ; 1st International Betaherpesvirus Workshop
Mjesto i datum
Maastricht, Nizozemska, 20.05.2003. - 25.05.2003
Vrsta sudjelovanja
Poster
Vrsta recenzije
Nije recenziran
Ključne riječi
STAT2; signaling
Sažetak
Cytomegaloviruses (CMVs) inhibit type I and type II interferon (IFN) receptor signaling through the JAK/STAT pathway and IFN-dependent expression of antiviral target genes. Based on a forward genetic procedure involving screening of a library of CMV mutants derived from random transposon mutagenesis by cis-acting reporter genes we identified the gene m27 of mouse CMV (MCMV) to mediate this effect. Expression of m27 prevented nuclear accumulation of STAT2 in infected cells and resulted in a rapid proteasome-dependent degradation of STAT2 but not STAT1. Isolated expression of m27 was sufficient to mediate these effects. Deletion of m27 conferred susceptibility of MCMV replication to IFN-a/b. Unexpectedly, m27 had a much more drastic effect on IFN-g mediated antiviral activities which was strictly dependent on STAT2 and was also contingent on IFN-a/bR1 expression. Replication of the m27MCMV mutant was dramatically attenuated in wildtype mice but partly restored in IFN-a/bR-deficient as well as IFN-gR-deficient mice. The results establish a new mechanism for viral immune escape and document an unforeseen biological significance of STAT2 in IFN-gR signaling. The data support a model of molecular cross-talk between IFN-g and IFN-a/b signaling components which requires STAT2.
Izvorni jezik
Engleski
