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anti-Mouse (Murine) STAT2 Antikörper:
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Human Monoclonal STAT2 Primary Antibody für IF, IP - ABIN967806
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 für IF, IP - ABIN967807
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 für 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 für 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 für 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 (zeige RNF2 Antikörper) promotes STAT1 (zeige STAT1 Antikörper)/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 (zeige IRF9 Antikörper)-independent signaling pathways but with reduced efficiency, with delayed and prolonged kinetics, and is more dependent on STAT1 (zeige STAT1 Antikörper) and STAT2 than IRF9 (zeige IRF9 Antikörper); and 2) signaling pathways not involving STAT1 (zeige STAT1 Antikörper), STAT2, or IRF9 (zeige IRF9 Antikörper) play a minor role only in mediating IFN-alpha (zeige IFNA Antikörper)-stimulated genes expression in MGCs.
transcriptional activation of Adar1 (zeige ADAR Antikörper) by IFN occurs in the absence of STAT1 (zeige STAT1 Antikörper) by a non-canonical STAT2-dependent pathway in mouse but not human cells.
IFN-alpha (zeige IFNA Antikörper)/beta is able to drive the formation of a Stat2 and IRF-9 (zeige IRF9 Antikörper) complex that drives the expression of a subset of IFN-stimulated genes, but with substantially delayed kinetics.
Activation of STAT2/IRF9 (zeige IRF9 Antikörper) induces a prolonged ISGF3 (zeige IRF9 Antikörper)-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.
propose that one molecule of C protein associates with the STAT1 (zeige STAT1 Antikörper):STAT2 heterodimer, inducing a conformational change to an antiparallel form, which is easily dephosphorylated
highlight the existence of a STAT1 (zeige STAT1 Antikörper)-independent IFN-I signaling pathway, where STAT2/IRF9 (zeige IRF9 Antikörper) can potentially substitute for the role of ISGF3 (zeige STAT1 Antikörper) 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 (zeige IFNA Antikörper) on hepatocellular carcinoma cell proliferation through activation of the JAK (zeige JAK3 Antikörper)/STAT (zeige STAT1 Antikörper) signaling pathway by inhibiting SOCS3 (zeige SOCS3 Antikörper) expression.
data suggest that STAT2 plays a role in the psoriasis pathogenesis by regulating the expression of CXCL11 (zeige CXCL11 Antikörper) and CCL5 (zeige CCL5 Antikörper), 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 (zeige TAZ Antikörper) domain of CREB binding protein (zeige CREBBP Antikörper) and the intrinsically disordered transactivation domain of STAT2 (TAD (zeige CRTAM Antikörper)-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.
Data show that moringin (GMG-ITC) had a limited inhibitory effect on IFNalpha-induced STAT1 (zeige STAT1 Antikörper) and STAT2 activity, indicating differentially targeting JAK (zeige JAK3 Antikörper)/STAT (zeige STAT1 Antikörper) signaling pathways.
study demonstrates that overexpression of Porcine deltacoronavirus (PDCoV) nsp5 (zeige SPECC1 Antikörper) also antagonizes IFN signaling by cleaving STAT2, an essential component of transcription factor complex ISGF3 (zeige STAT1 Antikörper), and that PDCoV infection reduces the levels of STAT2, which may affect the innate immune response
While La Piedad Michoacan Mexico Virus V protein does not affect the protein levels of STAT1 (zeige STAT1 Antikörper) or STAT2, it does prevent the interferon (zeige IFNA Antikörper)-induced phosphorylation and nuclear translocation of STAT1 (zeige STAT1 Antikörper) and STAT2 thereby inhibiting cellular responses to interferon alpha (zeige IFNA Antikörper)/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 (zeige STAT1 Antikörper)/STAT2 nuclear translocation.
Nsp1beta inhibits interferon-activated (zeige MNDA Antikörper) STAT1 (zeige STAT1 Antikörper)/STAT2 signal transduction by inducing karyopherin-alpha1 degradation.
the majority of the STAT1 (zeige STAT1 Antikörper)/STAT2/IRF9 (zeige IRF9 Antikörper) (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 (zeige STAT1 Antikörper) 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