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anti-Human STAT1 Antikörper:
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Human Monoclonal STAT1 Primary Antibody für ICS - ABIN1177190
Tanaka, Saito, Kunisawa, Kurashima, Wake, Suzuki, Shultz, Kiyono, Ishikawa: Development of mature and functional human myeloid subsets in hematopoietic stem cell-engrafted NOD/SCID/IL2rγKO mice. in Journal of immunology (Baltimore, Md. : 1950) 2012
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Human Polyclonal STAT1 Primary Antibody für CyTOF, FACS - ABIN4900633
Noser, Mael, Sakuma, Ohmine, Marcato, Lee, Ikeda: The RAS/Raf1/MEK/ERK signaling pathway facilitates VSV-mediated oncolysis: implication for the defective interferon response in cancer cells. in Molecular therapy : the journal of the American Society of Gene Therapy 2007
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Human Polyclonal STAT1 Primary Antibody für WB - ABIN1881847
Clarke, Clifford, Jindarat, Proud, Pang, Belvisi, Knox: TNFα and IFNγ synergistically enhance transcriptional activation of CXCL10 in human airway smooth muscle cells via STAT-1, NF-κB, and the transcriptional coactivator CREB-binding protein. in The Journal of biological chemistry 2010
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Human Polyclonal STAT1 Primary Antibody für IHC - ABIN967087
Schindler, Fu, Improta, Aebersold, Darnell: Proteins of transcription factor ISGF-3: one gene encodes the 91-and 84-kDa ISGF-3 proteins that are activated by interferon alpha. in Proceedings of the National Academy of Sciences of the United States of America 1992
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Human Polyclonal STAT1 Primary Antibody für IF (p), IHC (p) - ABIN674889
Wang, Wang, Song, Chu, Qu: Deficiency of interferon-gamma or its receptor promotes colorectal cancer development. in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 2015
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Human Monoclonal STAT1 Primary Antibody für IP - ABIN535279
Kovarik, Boudny, Kocak, Lauerova, Fait, Vagundova: Malignant melanoma associates with deficient IFN-induced STAT 1 phosphorylation. in International journal of molecular medicine 2003
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Human Polyclonal STAT1 Primary Antibody für IHC (p), ELISA - ABIN537760
Klampfer, Huang, Swaby, Augenlicht: Requirement of histone deacetylase activity for signaling by STAT1. in The Journal of biological chemistry 2004
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Polyclonal STAT1 Primary Antibody für ELISA, WB - ABIN539531
Ramsauer, Farlik, Zupkovitz, Seiser, Kröger, Hauser, Decker: Distinct modes of action applied by transcription factors STAT1 and IRF1 to initiate transcription of the IFN-gamma-inducible gbp2 gene. in Proceedings of the National Academy of Sciences of the United States of America 2007
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Polyclonal STAT1 Primary Antibody für ELISA, WB - ABIN539554
Soond, Carroll, Townsend, Sayan, Melino, Behrmann, Knight, Latchman, Stephanou: STAT1 regulates p73-mediated Bax gene expression. in FEBS letters 2007
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Human Polyclonal STAT1 Primary Antibody für IHC, WB - ABIN361958
Heim: The Jak-STAT pathway: cytokine signalling from the receptor to the nucleus. in Journal of receptor and signal transduction research 1999
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Study reports that MAGEA3 interacts with STAT1 and regulates the expression of tyrosine phosphorylated STAT1 (pY-STAT1) in tumor cells. MAGEA3 expression in tumor cells is associated with immune cells infiltration into tumor microenvironment and anti-tumor immune responses.
STAT1 Gain-of-Function and Dominant Negative STAT3 Mutations Impair IL-17 and IL-22 Immunity Associated with Chronic mucocutaneous candidiasis.
Alleles rs115662534(T) and rs548231435(C), Disrupt the Binding of Transcription Factors STAT1 and EBF1 to the Regulatory Elements of Human CD40 Gene
Here the authors describe the identification of gamma-activated site (GAS)-like, signal transducer and activator of transcription (STAT) binding elements (SBEs) within the proximal promoters of the MMP-1 and MMP-3 genes, which bind STAT-1 in a homodimer like complex (HDLC). They further demonstrate that MMP expression and binding of this complex to SBEs can be enhanced by interleukin (IL)-6.
STAT1 as a significant ETV6-NTRK3 (EN) fusion-regulated transcription factor and a crucial mediator of EN-induced tumorigenesis.
High expression of STAT1 in tumors was significantly associated with improved disease-free survival (P = 0.0256) and overall survival (P = 0.0193).
Integrin alpha5beta6 down-regulation causes a significant increase in donor cancer cells, and their exosomes, of two molecules that have a tumor suppressive role, STAT1 and MX1.
These results provide evidence for a novel cell cycle regulatory network in glioma comprising the Long non-coding PLAC2 along with STAT1 and RPL36.
ERK is an effective negative regulator of STAT1 signaling in esophageal squamous cell carcinoma, by promoting its proteasome degradation and decreasing IFNgamma production.
we suggest that STAT1HDAC4 signaling induces malignant tumor features such as EMT and sphere formation in CUG2overexpressing cancer cells.
Downregulated NDR1 protein kinase inhibits innate immune response by initiating an miR146a-STAT1 feedback loop.
High STAT1 expression is associated with Melanoma.
These results demonstrated that the IFNGinduced immunosuppressive properties of B7H1 in human BM and WJMSCs were mediated by STAT1 signaling, and not by PI3K/RACalpha serine/threonineprotein kinase signaling
STAT1 plays a pivotal role as a tumor suppressor in glioma.
the present study revealed a negative correlation between the expression of the STAT-1 gene and the glioma grade, as well as between STAT-1 and mutant p53 expression. The negative correlation between STAT-1 and the pathological level of glioma suggested that STAT-1 may be associated with the occurrence and development of glioma, and may be a diagnostic biomarker and therapeutic target for the malignancy of glioma.
PARP9 and PARP14 regulate macrophage activation in macrophage cell lines treated with either IFNgamma or IL-4; PARP14 silencing induces pro-inflammatory genes and STAT1 phosphorylation in M(IFNgamma) cells, whereas it suppresses anti-inflammatory gene expression and STAT6 phosphorylation in M(IL-4) cells
PVT1 interacts with STAT1 to inhibit IFN-alpha signaling and tumor cells proliferation.
STAT1 is associated with giant cell tumor of bone recurrence, which might serve as biomarker for giant cell tumor of bone recurrence
High STAT1 expression is associated with head and neck squamous cell carcinoma.
The research described here specifies where in the JAK/STAT signaling cascade the IFN response is inhibited and which protein domain of nsP2 is responsible for IFN inhibition. The results illuminate new aspects of antiviral defense and CHIKV counterdefense strategies and will direct the search for novel antiviral compounds.
SIRT2 deacetylates cyclin-dependent kinase 9 (CDK9) in a type I IFN-dependent manner and that the CDK9 deacetylation is essential for STAT1 phosphorylation at Ser-727.
Suppression of STAT1 activation shaped the functional identity and effector characteristics of memory CD4+ T cells.
The authors describe a critical role for STAT1 in promoting T-cell survival by maintaining sufficient MHC class I expression to evade NK cell-mediated killing.
High STAT1 expression is associated with resistance to Oncolytic Virotherapy in gliobalstoma.
propose a role for Intu in protecting cells and tissues after injury by targeting STAT1 for degradation and maintaining primary cilia
interferon-gamma-signal transducer and activator of transcription 1 (IFN-gamma-Stat1) pathway was required for generating colitogenic macrophages, given that Stat1-/- mice had less severe colitis and fewer colitogenic macrophages
Study in MMTV/MT6 and MMTV/NIC breast cancer mouse models show that ShcA phosphotyrosine motifs potentiate immune suppression by limiting signal transducer and activator of transcription (STAT)-1-driven anti-tumour immunity, while simultaneously increasing STAT3 immunosuppressive signals.
These findings provide mechanistic insight into how polymorphisms that attenuate NFKB1 expression predispose humans to epithelial cancers, highlighting the pro-tumorigenic activity of STAT1 and identifying targetable vulnerabilities in GC.
these data suggest that aloin attenuated LPSinduced inflammation by inhibiting ROSmediated activation of the JAK1STAT1/3 signalling pathway, thereby inhibiting the nuclear translocation of STAT1/3 in RAW264.7 cells.
STAT1 binds to the IL-22 promoter and directly antagonizes STAT3-mediated IL-22 induction.
These results reveal that STAT1 pS727 regulates growth and differentiation in JAK-STAT activated neoplasms and suggest that Mediator kinase inhibition represents a therapeutic strategy to regulate JAK-STAT signaling
Downregulated SOCS1 expression activates the JAK1/STAT1 pathway and promotes polarization of macrophages into M1 type.
The Lipopolysaccharide and IFN-beta-mediated increase of STAT1 mRNA and protein levels was abrogated by chelation of Zn(2+) with the membrane permeable chelator N,N,N',N'-Tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) in RAW 264.7 macrophages.
The possibility that the Gas6-Mer-PI3K/Akt-STAT1-LXR-Arg2 pathway plays an essential role for resolving inflammatory response in acute lung injury.
The results of this study strongly indicated that release of interferons by neuronal cells expressing polyglutamine-TBP leads to induction of STAT1 and consequent downregulation of miR-29a/b by a series of cell signaling events.
STAT1 is required to protect B cell development during murine norovirus infection.
Rigidity plays a key role in the toxicity of multi-walled carbon nanotubes and results in increased inflammatory, immunologic, and fibrogenic effects in the lung. STAT1 is an important protective factor in the fibroproliferative response to rMWCNTs, regulating both induced TGF-beta1 production and Smad2/3 phosphorylation status.
these results confirmed that myricitrin exhibited anti-inflammatory activity by blocking the activation of JAKs and the downstream transcription factor STAT1, which may result from the downregulation of NOX2-dependent ROS production mediated by myricitrin.
Collectively, these data show that porcine epidemic diarrhea virus is capable of subverting the type I interferon response by inducing STAT1 degradation.
this study shows that weaning caused severe inflammation associated with the suppression of STAT1 in the jejunum of piglets
Data indicate that transmissible gastroenteritis virus (TGEV) infection activates the janus kinase signal transducer and activator of the transcription 1 (JAK-STAT1) signaling pathway.
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/STAT2 nuclear translocation.
Nsp1beta inhibits interferon-activated STAT1/STAT2 signal transduction by inducing karyopherin-alpha1 degradation.
STAT1 is involved in mediating the action of ghrelin on ovarian cell functions.
the majority of the STAT1/STAT2/IRF9 (IFN regulatory factor 9) heterotrimers remained in the cytoplasm of PRRSV-infected cells, which indicates that the nuclear translocation of the heterotrimers was blocked
Cell-type-specific expression of STAT1 highlight the complex interplay between endometrium and conceptus for pregnancy recognition and implantation.
Nitric oxide-dependent increase in caspase-8 mRNA levels is associated with phosphorylation of STAT-1 at Ser-727 and STAT1 binding to the caspase-8 promoter in cultured lung endothelial cells.
Activated STAT1 may be associated with or perhaps contribute to the structural and inflammatory changes in pacing-induced sustained atrial fibrillation.
The tight junction protein ZO-2 is involved in regulation of vascular smooth muscle cells growth control upon vascular injury that is mediated by the transcription factor Stat1.
Report interferon-tau dependent STAT1 regulation of SOCS genes in bovine endometrium during estrus cycle and embryo implantation.
the interaction between STAT1 SNP and SNP19069 was highly significant for survival rate
results show for the first time that interleukin-6 (IL), in the presence of its soluble receptor (sIL-6R), induces activation of JAK1, JAK2, and STAT1/STAT3 proteins in bovine articular chondrocytes
Results from this study are consistent with previous studies on the role of STAT1 in regulating the transcription of genes involved in milk protein synthesis and fat metabolism.
Prolonged treatment with IFN-alpha (12-48 h) resulted in increased expression of STAT1 and, to a lesser extent, STAT2.
Study establishes a role for Stat4 in zebrafish great vessel development, and suggests that Stat4 may serve as a therapeutic target for great vessels defects.
The role of stat1b in zebrafish hematopoiesis.
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. This protein can be activated by various ligands including interferon-alpha, interferon-gamma, EGF, PDGF and IL6. This protein mediates the expression of a variety of genes, which is thought to be important for cell viability in response to different cell stimuli and pathogens. Two alternatively spliced transcript variants encoding distinct isoforms have been described.
signal transducer and activator of transcription 1-alpha/beta
, signal transducer and activator of transcription-1
, transcription factor ISGF-3 components p91/p84
, signal transducer and activator of transcription 1
, signal transducer and activator of transcription 4
, transcription factor ISGF-3
, activator of transcription
, signal transduction
, LOW QUALITY PROTEIN: signal transducer and activator of transcription 1-alpha/beta
, signal transducer and activator of transcription 1, 91kDa
, signal transduction and activation of transcription 1
, signal transduction and activation of transcription 1a