-
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.
-
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.
-
Data suggest that histone acetylation drives elevated Stat1/Myd88 expression in macrophages from mice with type 1 diabetes; this mechanism is exhibited in both peritoneal macrophages and bone marrow-differentiated macrophages. (Stat1 = signal transducer and activator of transcription 1; Myd88 = myeloid differentiation primary response gene 88)
-
the role of unphosphorylated STAT1 differs from that of P-STAT1, and represses apoptosis in macrophages to promote immune evasion during Mycobacterium tuberculosis infection.
-
Data show that RNF2 promotes STAT1/STAT2 disassociation from DNA.
