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The full length cDNA sequence of Atlantic salmon (Salmo salar) ssSTAT2 was determined and phylogenetic analysis of the amino acid sequence grouped this novel salmon gene to the STAT2 clade.
transcriptional activation of Adar1 (show ADAR ELISA Kits) by IFN occurs in the absence of STAT1 (show STAT1 ELISA Kits) by a non-canonical STAT2-dependent pathway in mouse but not human cells.
IFN-alpha (show IFNA ELISA Kits)/beta is able to drive the formation of a Stat2 and IRF-9 (show IRF9 ELISA Kits) complex that drives the expression of a subset of IFN-stimulated genes, but with substantially delayed kinetics.
Activation of STAT2/IRF9 (show IRF9 ELISA Kits) induces a prolonged ISGF3 (show IRF9 ELISA Kits)-like transcriptome and generates an antiviral response.
In a mouse syngeneic tumor transplantation model STAT2 expression reduces tumor growth.
Data suggest a role for Vc in Nanog regulation networks and reveal a novel role for STAT2 in regulating Nanog expression.
Stat2 loss leads to reduced expression of NF-kappaB (show NFKB1 ELISA Kits) target genes by affecting nuclear translocation of NF-kappaB (show NFKB1 ELISA Kits).
STAT1 (show STAT1 ELISA Kits), not STAT2 or IRF9 (show IRF9 ELISA Kits), prevent the emergence of a lethal antiviral CD4 (show CD4 ELISA Kits)(+) T-cell response after lymphocytic choriomeningitis virus infection.
Activation of Oas1a gene expression by type I IFN requires both STAT1 (show STAT1 ELISA Kits) and STAT2.
In a constructive process, pM27 recruits DDB1 (show DDB1 ELISA Kits) to exploit ubiquitin ligase (show RNF123 ELISA Kits) complexes catalyzing the obstruction of the STAT2-dependent antiviral state of cells to permit viral replication.
NS5 (show RAF1 ELISA Kits) is able to bind and degrade human STAT2, but not mouse STAT2; demonstrate that mouse STAT2 restricts early dengue virus replication in vivo
These results establish that activation of STAT (show STAT1 ELISA Kits) pathway is essential for anti-hepatitis c virus efficacy of IFN-alpha (show IFNA ELISA Kits).
These findings indicate that overexpression of IFITM1 enhances the aggressive phenotype of triple-negative SUM149 IBC cells and that this effect is dependent on STAT2/BRG1 (show SMARCA4 ELISA Kits) interaction.
These results suggest that STAT6 (show STAT6 ELISA Kits) plays an important role in regulating Sp1 (show PSG1 ELISA Kits) and BCL6 (show BCL6 ELISA Kits) through STAT2 to exert the anti-proliferative effects of type I IFN.
Interferonstimulated gene factor 3 complex, which consists of STAT1 (show STAT1 ELISA Kits), STAT2 and IRF9 (show IRF9 ELISA Kits), is required for the induction of SAMHD1 (show SAMHD1 ELISA Kits) expression by IFN-alpha (show IFNA ELISA Kits) in SMMC-7721 cells.
IFN-beta (show IFNB1 ELISA Kits) exhibited significant cytotoxicity in HepG2 cells mainly through phosphorylation of STAT2.
STAT2 rs2066807 polymorphism is not associated with cervical cancer.
Influenza virus-infected cells respond with increased induction of interferon beta (show IFNB1 ELISA Kits) upon Staphylococcus aureus super-infection, however, subsequent interferon (show IFNA ELISA Kits)-stimulated gene expression are rather impaired due to a block of STAT1 (show STAT1 ELISA Kits)-STAT2 dimerization.
The results demonstrated that Peste-des (show DES ELISA Kits)-petits-ruminants virus V protein blocks interferon (show IFNA ELISA Kits) actions in a dose dependent manner and restrains the translocation of STAT1 (show STAT1 ELISA Kits)/2 proteins.
Respiratory syncytial virus NS1 (show PTPN11 ELISA Kits) upregulates SOCS1 (show SOCS1 ELISA Kits) expression in a RIG-I (show DDX58 ELISA Kits)- and TLR3 (show TLR3 ELISA Kits)-independent pathway, to inhibit STAT2 phosphorylation.
While La Piedad Michoacan Mexico Virus V protein does not affect the protein levels of STAT1 (show STAT1 ELISA Kits) or STAT2, it does prevent the interferon (show IFNA ELISA Kits)-induced phosphorylation and nuclear translocation of STAT1 (show STAT1 ELISA Kits) and STAT2 thereby inhibiting cellular responses to interferon alpha (show IFNA ELISA Kits)/beta.
Taken together, results of these experiments describe for the first time a novel mechanism by which foot-and-mouth disease virus evolves to inhibit IFN signaling via blocking STAT1 (show STAT1 ELISA Kits)/STAT2 nuclear translocation.
Nsp1beta inhibits interferon-activated STAT1 (show STAT1 ELISA Kits)/STAT2 signal transduction by inducing karyopherin-alpha1 degradation.
the majority of the STAT1 (show STAT1 ELISA Kits)/STAT2/IRF9 (show IRF9 ELISA Kits) (IFN regulatory factor 9) heterotrimers remained in the cytoplasm of PRRSV-infected cells, which indicates that the nuclear translocation of the heterotrimers was blocked
Prolonged treatment with IFN-alpha (12-48 h) resulted in increased expression of STAT1 (show STAT1 ELISA Kits) and, to a lesser extent, STAT2.
The protein encoded by this gene is a member of the STAT protein family. In response to cytokines and growth factors, STAT family members are phosphorylated by the receptor associated kinases, and then form homo- or heterodimers that translocate to the cell nucleus where they act as transcription activators. In response to interferon (IFN), this protein forms a complex with STAT1 and IFN regulatory factor family protein p48 (ISGF3G), in which this protein acts as a transactivator, but lacks the ability to bind DNA directly. Transcription adaptor P300/CBP (EP300/CREBBP) has been shown to interact specifically with this protein, which is thought to be involved in the process of blocking IFN-alpha response by adenovirus. Multiple transcript variants encoding different isoforms have been found for this gene.
, signal transducer and activator of transcription 2
, signal transducer and activator of transcription (AGAP000099-PA)
, interferon alpha induced transcriptional activator