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Results indicate that pSTAT1 positivity is a potential biomarker for patient with breast cancer, since pSTAT1 positivity significantly reflects PDL1 and HLA class I expressions on tumor cells as well as PDL1 expression on tumorinfiltrating CD8positive T cells.
The level of p-JAK2 and p-STAT1 increased after FRK overexpression, while they decreased after FRK downregulation both in U251 and U87 cells. However, FRK had no effect on STAT3 phosphorylation. FRK-induced STAT1 activation was not dependent on JAK2. FRK associated with STAT1, induced STAT1 nuclear translocation and regulated the expressions of STAT1-related target genes.
A significant positive correlation was demonstrated between STAT1 and STAT2 and also between STAT1 and STAT3.
Together these results indicate that IRF1 promotes DNA binding of STAT1, which can in turn participate in a positive feedback loop of JAK-STAT signaling.
These data suggest that the JAK2/STAT1 pathway in TNBC might regulate the dynamic expression of PD-L1 that is induced in the setting of an inflammatory response
data indicate that Hematopoietic stem cell transplantation for patients with GOF-STAT1 mutations is curative but has significant risk of secondary graft failure and death.
Description of the role of inherited STAT1 and STAT3 mutations in the setting of human disease with highly variable phenotypes that include immunodeficiency, malignancy, and autoimmunity (review).
Study discovered that HCMV-induced STAT1 helps direct motility, differentiation, and polarization of infected monocytes. These results suggest the identification of a proviral outcome for the activation of the traditionally antiviral player, STAT1, during HCMV infection of monocytes.
Activated TYK2 leads to STAT1 and STAT3 phosphorylation, activated expression of MCL1 and aberrant ALCL cell survival.
pharmacological inhibition of eIF4A, the RNA helicase component of eIF4F, elicits powerful antitumor immune-mediated effects via PD-L1 downregulation. Thus, eIF4A inhibitors, in development as anticancer drugs, may also act as cancer immunotherapies.
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.
These data demonstrate that epithelial STAT1 is a male-specific tumor suppressor in colorectal cancer of mice and humans.
The proatherosclerotic effects of tumor necrosis factor (ligand) superfamily member 12 (TWEAK) were mediated, at least in part, by signal transducer and activator of transcription 1 (STAT1) activation and expression of proinflammatory target genes.
Defective STAT1 activation in Casp11(-/-) colons during disease progression.
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.
Downregulated NDR1 protein kinase inhibits innate immune response by initiating an miR146a-STAT1 feedback loop.
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.
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
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.
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