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001-es BibID:	BIBFORM063693
Első szerző:	Blaszczyk, Katarzyna
Cím:	STAT2/IRF9 directs a prolonged ISGF3-like transcriptional response and antiviral activity in the absence of STAT1 / Katarzyna Blaszczyk, Adam Olejnik, Hanna Nowicka, Lilla Ozgyin, Yi-Ling Chen, Stefan Chmielewski, Kaja Kostyrko, Joanna Wesoly, Balint Laszlo Balint, Chien-Kuo Lee, Hans A. R. Bluyssen
Dátum:	2015
ISSN:	0264-6021
Megjegyzések:	Evidence is accumulating for the existence of a signal transducer and activator of transcription 2 (STAT2)/interferon regulatory factor 9 (IRF9)-dependent, STAT1-independent interferon alpha (IFN?) signalling pathway. However, no detailed insight exists into the genome-wide transcriptional regulation and the biological implications of STAT2/IRF9-dependent IFN? signalling as compared with interferon-stimulated gene factor 3 (ISGF3). In STAT1-defeicient U3C cells stably overexpressing human STAT2 (hST2-U3C) and STAT1-deficient murine embryonic fibroblast cells stably overexpressing mouse STAT2 (mST2-MS1KO) we observed that the IFN?-induced expression of 2'-5'-oligoadenylate synthase 2 (OAS2) and interferon-induced protein with tetratricopeptide repeats 1 (Ifit1) correlated with the kinetics of STAT2 phosphorylation, and the presence of a STAT2/IRF9 complex requiring STAT2 phosphorylation and the STAT2 transactivation domain. Subsequent microarray analysis of IFN?-treated wild-type (WT) and STAT1 KO cells overexpressing STAT2 extended our observations and identified ?120 known antiviral ISRE-containing interferon-stimulated genes (ISGs) commonly up-regulated by STAT2/IRF9 and ISGF3. The STAT2/IRF9-directed expression profile of these IFN-stimulated genes (ISGs) was prolonged as compared with the early and transient response mediated by ISGF3. In addition, we identified a group of 'STAT2/IRF9-specific' ISGs, whose response to IFN? was ISGF3-independent. Finally, STAT2/IRF9 was able to trigger an antiviral response upon encephalomyocarditis virus (EMCV) and vesicular stomatitis Indiana virus (VSV). Our results further prove that IFN?-activated STAT2/IRF9 induces a prolonged ISGF3-like transcriptome and generates an antiviral response in the absence of STAT1. Moreover, the existence of 'STAT2/IRF9-specific' target genes predicts a novel role of STAT2 in IFN? signalling.
Tárgyszavak:	Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Biochemical Journal. - 466 : 3 (2015), p. 511-524. -
További szerzők:	Olejnik, Adam Nowicka, Hanna Ozgyin Lilla (1989-) (molekuláris biológus) Chen, Yi-Ling Chmielewski, Stefan Kostyrko, Kaja Wesoly, Joanna Bálint Bálint László (1971-) (kutató orvos) Lee, Chien-Kuo Bluyssen, Hans A. R.
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