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anti-Mouse (Murine) STAT2 Antibodies:
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Human Monoclonal STAT2 Primary Antibody for IF, IP - ABIN967806
Blesofsky, Mowen, Arduini, Baker, Murphy, Bowtell, David: Regulation of STAT protein synthesis by c-Cbl. in Oncogene 2001
Show all 5 references for ABIN967806
Human Polyclonal STAT2 Primary Antibody for IHC (p), WB - ABIN319409
Schamel, Reth: Monomeric and oligomeric complexes of the B cell antigen receptor. in Immunity 2000
Show all 4 references for ABIN319409
Human Polyclonal STAT2 Primary Antibody for WB - ABIN871439
Yan, Qureshi, Zhong, Wen, Darnell: The genomic structure of the STAT genes: multiple exons in coincident sites in Stat1 and Stat2. in Nucleic acids research 1995
Show all 4 references for ABIN871439
Human Polyclonal STAT2 Primary Antibody for EIA, IHC (p) - ABIN357081
Rodriguez, Wang, Horvath: Hendra virus V protein inhibits interferon signaling by preventing STAT1 and STAT2 nuclear accumulation. in Journal of virology 2003
Show all 2 references for ABIN357081
Human Monoclonal STAT2 Primary Antibody for WB - ABIN967579
Bromberg, Darnell: The role of STATs in transcriptional control and their impact on cellular function. in Oncogene 2000
Show all 2 references for ABIN967579
Human Polyclonal STAT2 Primary Antibody for FACS - ABIN4898096
Thacker, Berthier, Mattinzoli, Rastaldi, Kretzler, Kaplan: The detrimental effects of IFN-α on vasculogenesis in lupus are mediated by repression of IL-1 pathways: potential role in atherogenesis and renal vascular rarefaction. in Journal of immunology (Baltimore, Md. : 1950) 2010
Human Polyclonal STAT2 Primary Antibody for EIA, WB - ABIN401443
Li, Leung, Kerr, Stark: Functional subdomains of STAT2 required for preassociation with the alpha interferon receptor and for signaling. in Molecular and cellular biology 1997
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.
IFN-I can mediate ISG expression inmixed glial cell cultures (MGCs) via ISGF3 (show IRF9 Antibodies)-independent signaling pathways but with reduced efficiency, with delayed and prolonged kinetics, and is more dependent on STAT1 (show STAT1 Antibodies) and STAT2 than IRF9 (show IRF9 Antibodies); and 2) signaling pathways not involving STAT1 (show STAT1 Antibodies), STAT2, or IRF9 (show IRF9 Antibodies) play a minor role only in mediating IFN-alpha (show IFNA Antibodies)-stimulated genes expression in MGCs.
transcriptional activation of Adar1 (show ADAR Antibodies) by IFN occurs in the absence of STAT1 (show STAT1 Antibodies) by a non-canonical STAT2-dependent pathway in mouse but not human cells.
IFN-alpha (show IFNA Antibodies)/beta is able to drive the formation of a Stat2 and IRF-9 (show IRF9 Antibodies) complex that drives the expression of a subset of IFN-stimulated genes, but with substantially delayed kinetics.
Activation of STAT2/IRF9 (show IRF9 Antibodies) induces a prolonged ISGF3 (show IRF9 Antibodies)-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 Antibodies) target genes by affecting nuclear translocation of NF-kappaB (show NFKB1 Antibodies).
STAT1 (show STAT1 Antibodies), not STAT2 or IRF9 (show IRF9 Antibodies), prevent the emergence of a lethal antiviral CD4 (show CD4 Antibodies)(+) T-cell response after lymphocytic choriomeningitis virus infection.
Activation of Oas1a gene expression by type I IFN requires both STAT1 (show STAT1 Antibodies) and STAT2.
In a constructive process, pM27 recruits DDB1 (show DDB1 Antibodies) to exploit ubiquitin ligase (show RNF123 Antibodies) complexes catalyzing the obstruction of the STAT2-dependent antiviral state of cells to permit viral replication.
STAT2 recruits USP18 (show USP18 Antibodies) to the type I IFN receptor subunit IFNAR2 (show IFNAR2 Antibodies) via its constitutive membrane-distal STAT2-binding site.
These results establish that activation of STAT (show STAT1 Antibodies) pathway is essential for anti-hepatitis c virus efficacy of IFN-alpha (show IFNA Antibodies).
These findings indicate that overexpression of IFITM1 (show IFITM1 Antibodies) enhances the aggressive phenotype of triple-negative SUM149 IBC cells and that this effect is dependent on STAT2/BRG1 (show SMARCA4 Antibodies) interaction.
These results suggest that STAT6 (show STAT6 Antibodies) plays an important role in regulating Sp1 (show PSG1 Antibodies) and BCL6 (show BCL6 Antibodies) through STAT2 to exert the anti-proliferative effects of type I IFN.
Interferonstimulated gene factor 3 complex, which consists of STAT1 (show STAT1 Antibodies), STAT2 and IRF9 (show IRF9 Antibodies), is required for the induction of SAMHD1 (show SAMHD1 Antibodies) expression by IFN-alpha (show IFNA Antibodies) in SMMC-7721 cells.
IFN-beta (show IFNB1 Antibodies) 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 Antibodies) upon Staphylococcus aureus super-infection, however, subsequent interferon (show IFNA Antibodies)-stimulated gene expression are rather impaired due to a block of STAT1 (show STAT1 Antibodies)-STAT2 dimerization.
The results demonstrated that Peste-des (show DES Antibodies)-petits-ruminants virus V protein blocks interferon (show IFNA Antibodies) actions in a dose dependent manner and restrains the translocation of STAT1 (show STAT1 Antibodies)/2 proteins.
While La Piedad Michoacan Mexico Virus V protein does not affect the protein levels of STAT1 (show STAT1 Antibodies) or STAT2, it does prevent the interferon (show IFNA Antibodies)-induced phosphorylation and nuclear translocation of STAT1 (show STAT1 Antibodies) and STAT2 thereby inhibiting cellular responses to interferon alpha (show IFNA Antibodies)/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 Antibodies)/STAT2 nuclear translocation.
Nsp1beta inhibits interferon-activated (show MNDA Antibodies) STAT1 (show STAT1 Antibodies)/STAT2 signal transduction by inducing karyopherin-alpha1 degradation.
the majority of the STAT1 (show STAT1 Antibodies)/STAT2/IRF9 (show IRF9 Antibodies) (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 Antibodies) 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