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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 (show WNT2 Proteins)-beta-catenin (show CTNNB1 Proteins)-dependent manner.
Colorectal carcinoma cells induce M2 polarization of tumor-associated macrophagess through MFHAS1 induction and subsequent STAT6 and KLF4 (show KLF4 Proteins) activation to promote CRC progression.
Our results demonstrate that STAT6 is critical in the early steps of colitis-associated colon cancer (CAC (show SLC25A20 Proteins)) development for modulating inflammatory responses and controlling cell recruitment and proliferation. Thus, STAT6 may represent a promising target for CAC (show SLC25A20 Proteins) 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 (show STAT3 Proteins), STAT6 and/or SMAD3 (show SMAD3 Proteins) 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 (show WNT2 Proteins) signaling pathway
These data indicate a role for STAT3 (show STAT3 Proteins) 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.
these results showed that allergy responses further accelerated the IL-4 (show IL4 Proteins)-induced inhibition of tumor development through the activation of STAT6 pathways.
In this study, significant lower level of miR (show MLXIP Proteins)-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 (show STAT3 Proteins) was the potential treated target for breast cancer therapy, whereas STAT5A (show STAT5A Proteins)/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 (show TNFSF11 Proteins) 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 (show TNFSF11 Proteins). (STAT6 = signal transducer and activator of transcription 6; RANKL (show TNFSF11 Proteins) = receptor activator of nuclear factor kappa B ligand (show TNFSF11 Proteins))
The results showed that SARS (show SARS Proteins) coronavirus papain-like protease (PLPro) stimulated TGF-beta1 (show TGFB1 Proteins)-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 (show FCER2 Proteins) expression, 1p36/TNFRSF14 (show TNFRSF14 Proteins) 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.
this study shows that weaning caused severe inflammation associated with the suppression of STAT6 in the jejunum of piglets
Data show that IL-4 (show IL4 Proteins) induces upregulation of the junction protein claudin-5 (show CLDN5 Proteins) in endothelial cells (ECs) through activation of Jak (show JAK3 Proteins)/STAT6 and phosphorylation and translocation of FoxO1 (show FOXO1 Proteins) from the nucleus to the cytoplasm.
Results provide evidence that polymorphisms in STAT6 are associated with carcass and growth efficiency traits
IL-4 (show IL4 Proteins) 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