Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Weitere Synonyme anzeigen
Wählen Sie die gewünschte Spezies
STAT6 signaling negatively affects permeability barrier function in vivo, even in the physiological state.
Our study demonstrates that STAT6 deficiency dysregulates the macrophage response to inflammatory outbursts by increasing the presence of a population of CD16+ macrophages that seems to contribute to intestinal fibrosis.
inhibition of the Stat6 pathway in Tumor-associated macrophages (TAMs) is a vital therapeutic approach to attenuate tumor growth and metastasis by inhibiting TAM-induced protumorigenic and prometastatic activities
IL-4/ STAT6 signaling needs to be well adjusted to ensure proper development and function of homing Th2 cells.
These results provide the first evidence that STAT6 affects depressive-like behavior through downregulating monoamines, including dopamine and 5-HT in the hippocampus of brain
IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli
IL-4Delta2 did not compete with IL-4 for IL-4Ralpha binding and did not interfere with the downstream STAT-6 phosphorylation in T cells.
Histamine and Stat6 have roles in differentiation of macrophages from CD11b(+) myeloid cells and formation of foam cells
IL-4Ralpha deficiency inhibited the activation of STAT6 in the mouse kidneys in two experimental models of renal fibrosis. . In vitro, IL-4 activated STAT6 and stimulated expression of alpha-smooth muscle actin and fibronectin in mouse bone marrow monocytes.
a T cell-specific Stat6/Pten axis links cold exposure or ADRB3 stimulation with Foxp3(+) Treg induction and adipose tissue function.
these findings show that Stat6 has an oncogenic role in intestinal tumorigenesis by promoting polyp cell proliferation and immunosuppressive mediators, and preventing an active cytotoxic process.
STAT6 facilitated atherosclerotic plaque stabilization by promoting the polarization of macrophages to M2 subtype and antagonizing ox-LDL-induced cell apoptosis and lipid deposition in a Wnt-beta-catenin-dependent manner.
Colorectal carcinoma cells induce M2 polarization of tumor-associated macrophagess through MFHAS1 induction and subsequent STAT6 and KLF4 activation to promote CRC progression.
Our results demonstrate that STAT6 is critical in the early steps of colitis-associated colon cancer (CAC) development for modulating inflammatory responses and controlling cell recruitment and proliferation. Thus, STAT6 may represent a promising target for CAC treatment.
Gefitinib effectively inhibits tumor-associated macrophage M2-like polarization both in vitro and in vivo by targeting the STAT6 signaling pathway.
M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 effectively restrict tumor growth. The findings justify the development of new anti-tumor cell therapy technology.
cytokine-activated STAT3 and STAT6 cooperate in macrophages to promote a secretory phenotype that enhances tumor progression in a cathepsin-dependent manner.
these results demonstrate that a STAT6-dependent macrophage phenotype promotes mucosal repair in murine inflammatory bowel disease through activation of the Wnt signaling pathway
These data indicate a role for STAT3 in maintaining a steady state in the beta-cell, by modulating its cell cycle and protection from DNA damage.
STAT6 phosphorylation (p-STAT6) was significantly increased in TECs from both Grave's disease patients and experimental autoimmune Graves' disease mice.
the degradation of STAT6 is induced and required for the lytic activation of human herpesviruses and is association with the increased ubiquitylated form of TRIML2
the statistically significant association between STAT6 polymorphisms with intrinsic (non-atopic) asthma in Pakistani population, is reported.
AG1024+U0126 acted synergistically to downregulate "synergy" genes, especially STAT6 and PDAP1, which displayed significant expression codependency and a common expression pattern linked with other key "synergy" genes, supporting their predicted role in an STAT6-ERK-nuclear factor kappa beta (NF-kappaB) network. STAT6 loss impinges on the cell cycle, reducing viable cell count. Stat6 increased daunorubicin's cell killing.
is a dependable marker to differentiate solitary fibrous tumors and myofibromas
Inhibition of STAT6/Anoctamin-1 activation decreased proliferation, migration, or invasion of gastric cancer cells.
Results of our structure-function studies on STAT6 shed light on mechanism of DNA recognition by STATs in general and explain the reasons underlying STAT6's preference for N4 site DNA over N3.
There was no significant relationship between rs324011 and rs3024974 SNPs and psoriasis in the present study or in other studies, indicating that STAT6 is not a candidate gene for psoriasis susceptibility
these results showed that allergy responses further accelerated the IL-4-induced inhibition of tumor development through the activation of STAT6 pathways.
In this study, significant lower level of miR-214-3p and higher level of STAT6 in the intestinal mucosa of active UC patients compared with the health controls were confirmed by quantitative real-time PCR.
IL-13, IL-13Ralpha1, STAT6 and ZEB1 have roles in promoting epithelial-mesenchymal transition and aggressiveness of colorectal cancer cells
Our finding supports that STAT3 was the potential treated target for breast cancer therapy, whereas STAT5A/5B/6 were potential prognostic markers for better survival of BC, providing more accurate prognosis.
N4 DNA recognition by STAT6: structural and functional implications.
Data suggest that STAT6 and RANKL are involved in regulation of apoptosis, gene expression, and cell proliferation in hepatocellular carcinoma cell lines; depletion of STAT6 using RNA interference increases apoptosis; this mechanism involves down-regulation of expression of RANKL. (STAT6 = signal transducer and activator of transcription 6; RANKL = receptor activator of nuclear factor kappa B ligand)
The results showed that SARS coronavirus papain-like protease (PLPro) stimulated TGF-beta1-dependent expression of Type I collagen via activating STAT6 pathway.
High STAT6 expression is associated with melanoma.
Report a variant of t(14;18) negative nodal diffuse follicular lymphoma with CD23 expression, 1p36/TNFRSF14 abnormalities, and STAT6 mutations.
Our data indicate that hypoxic inhibition of JMJD3 activity reduces demethylation of H3K27me3, nucleosome removal, and hence induction of the STAT6 target gene CCL18, while induction of other STAT6-inducible genes such as SPINT2 remained unaffected by JMJD3.
The results suggest that nuclear localization and cleavage of STAT6 is important for modulating the viral latency and pathogenesis of Kaposi's sarcoma-associated herpesvirus (KSHV).
the phosphorylation of signal transducer and activator of transcription 1 (STAT1-py) was impaired in asthmatics, whereas the phosphorylation of signal transducer and activator of transcription 6 (STAT6-py) was slightly enhanced.
PVT1-derived miR-1207-5p promotes the proliferation of breast cancer cells by targeting STAT6.
this study shows that weaning caused severe inflammation associated with the suppression of STAT6 in the jejunum of piglets
Data show that IL-4 induces upregulation of the junction protein claudin-5 in endothelial cells (ECs) through activation of Jak/STAT6 and phosphorylation and translocation of FoxO1 from the nucleus to the cytoplasm.
Results provide evidence that polymorphisms in STAT6 are associated with carcass and growth efficiency traits
IL-4 and STAT6 are related to the pathogenesis of allergic rhinitis and may be the main factors for eosinophil infiltration in allergic rhinitis.
The protein encoded by this gene is a member of the STAT family of transcription factors. 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 plays a central role in exerting IL4 mediated biological responses. It is found to induce the expression of BCL2L1/BCL-X(L), which is responsible for the anti-apoptotic activity of IL4. Knockout studies in mice suggested the roles of this gene in differentiation of T helper 2 (Th2) cells, expression of cell surface markers, and class switch of immunoglobulins. Alternative splicing results in multiple transcript variants.
signal transducer and transcription activator 6
, STAT, interleukin4-induced
, signal transducer and activator of transcription 6
, transcription factor IL-4 STAT