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anti-Mouse (Murine) STAT2 Antibodies:
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Human Monoclonal STAT2 Primary Antibody for IF, IP - ABIN967807
Blesofsky, Mowen, Arduini, Baker, Murphy, Bowtell, David: Regulation of STAT protein synthesis by c-Cbl. in Oncogene 2001
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Human Monoclonal STAT2 Primary Antibody for IF, IP - ABIN967806
Duff, Quinlan, Paxton, Naik, Caughman: Pervanadate mimics IFNgamma-mediated induction of ICAM-1 expression via activation of STAT proteins. in The Journal of investigative dermatology 1997
Show all 5 Pubmed References
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 Pubmed References
Human Polyclonal STAT2 Primary Antibody for WB - ABIN223186
Dolniak, Katsoulidis, Carayol, Altman, Redig, Tallman, Ueda, Watanabe-Fukunaga, Fukunaga, Platanias: Regulation of arsenic trioxide-induced cellular responses by Mnk1 and Mnk2. in The Journal of biological chemistry 2008
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
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.
Data show that RNF2 (show RNF2 Antibodies) promotes STAT1 (show STAT1 Antibodies)/STAT2 disassociation from DNA.
this study shows that STAT2 plays a critical role in TLR-induced dendritic cell activation and cross-presentation, and
this study shows that STAT2 plays a critical role in TLR-induced dendritic cell activation and cross-presentation
these studies identify phosphorylation of S734-STAT2 as a new regulatory mechanism that negatively controls the type I IFN-antiviral response.
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.
Based on the proposition that NS5 (show RAF1 Antibodies) utilizes SIAH2 (show SIAH2 Antibodies)-mediated proteasomal degradation of STAT2, an in-silico study was carried out to characterize the protein-protein interactions between NS5 (show RAF1 Antibodies), SIAH2 (show SIAH2 Antibodies) and STAT2 proteins.
The pathways related to tumorigenicity and tumor progression, STAT2 and AdipoR1 (show ADIPOR1 Antibodies)/AMPK (show PRKAA1 Antibodies)/SIRT1 (show SIRT1 Antibodies) could be restrained by miR (show MLXIP Antibodies)-3908. In conclusion, restoration of miR (show MLXIP Antibodies)-3908 expression induced suppression of cancer progression and glioblastoma tumorigenicity.
propose that one molecule of C protein associates with the STAT1 (show STAT1 Antibodies):STAT2 heterodimer, inducing a conformational change to an antiparallel form, which is easily dephosphorylated
highlight the existence of a STAT1 (show STAT1 Antibodies)-independent IFN-I signaling pathway, where STAT2/IRF9 (show IRF9 Antibodies) can potentially substitute for the role of ISGF3 (show STAT1 Antibodies) and offer a back-up response against viral infection.
Decreased phosphorylated STAT2 expression was accompanied by increased replication of hepatitis C virus and hepatitis E virus.
6-Hydroxy-3-O-methyl-kaempferol 6-O-glucopyranoside potentiated the inhibitory effect of IFN-alpha (show IFNA Antibodies) on hepatocellular carcinoma cell proliferation through activation of the JAK (show JAK3 Antibodies)/STAT (show STAT1 Antibodies) signaling pathway by inhibiting SOCS3 (show SOCS3 Antibodies) expression.
data suggest that STAT2 plays a role in the psoriasis pathogenesis by regulating the expression of CXCL11 (show CXCL11 Antibodies) and CCL5 (show CCL5 Antibodies), and thereby attracting IFNgamma-producing immune cells to the skin
Interferon-alpha-enhanced IL-10 expression in human CD4 T cells is regulated by STAT3, STAT2, and BATF transcription factors.
the rate-limiting transition state for binding between the TAZ1 (show TAZ Antibodies) domain of CREB binding protein (show CREBBP Antibodies) and the intrinsically disordered transactivation domain of STAT2 (TAD (show CRTAM Antibodies)-STAT2) by site-directed mutagenesis and kinetic experiments (Phi-value analysis) and found that the native protein-protein binding interface is not formed at the transition state for binding.
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