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Validated All-in-One™ qPCR Primer for STAT6(NM_001178079.2) Search again
Product ID:
HQP161411
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
D12S1644, IL-4-STAT, STAT6B, STAT6C
Gene Description:
signal transducer and activator of transcription 6
Target Gene Accession:
NM_001178079.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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. [provided by RefSeq].
Gene References into function
- IL-4-dependent Stat6 activation is inhibited by an intracellularly delivered peptide derived from the Stat6-binding region of IL-4Ralpha.
- role in mediating responses of bronchial epithelium to cytokines in asthmatics
- Oligonucleotide fishing for STAT6: cross-talk between IL-4 and chemokines.
- STAT6 polymorphism is associated with increase in eosinophil cell count contributing to the pathogenesis of Asthma
- 3'UTR polymorphism is associated with susceptibility and severity in nut allergic patients
- STAT6 is required for IL-4-mediated growth inhibition and induction of apoptosis in human breast cancer cells.
- STAT6 has a protein binding motif that controls the interaction with NcoA-1 in transcriptional activation
- These results show that p38 MAPK provides a costimulatory signal for IL-4-induced gene responses by directly stimulating the transcriptional activation of STAT6.
- These findings identify p100 as a novel coactivator for STAT6 and suggest that p100 functions as a bridging factor between STAT6 and the basal transcription machinery.
- Protein phosphatase 2A (PP2A) regulates interleukin-4-mediated signaling by this protein.
- regulation of dephosphorylation by of mitogen-activated protein kinase and myosin light chain kinase
- IL-4-induced Stat6 signaling is a polygenic quantitative trait regulated by a collection of several contributing genetic loci.
- when osteoclastogenesis was induced independently of RANKL by using TNF-alpha, IL-4 inhibited osteoclast differentiation through a STAT6-dependent mechanism
- Characterization of the IL-4-responsive enhanceosome of the human polymeric Ig receptor gene demonstrates cooperation of STAT6, HNF1 and additional DNA-binding factors in mediating IL-4 responsiveness in HT-29 cells.
- These results suggest that MIP-T3 is a novel inhibitor of IL-13 signaling and may be a useful molecule in ameliorating various conditions in which IL-13 plays a central role.
- the Stat6 TAD contributes to promoter specificity by the differential recruitment of and requirement for a p160-class coactivator
- STAT6 is required for IL-4-IL-13-dependent SOCS-1 expression in A549 human lung adenocarcinoma cells; three identified STAT6-binding motifs in the SOCS-1 promoter cooperate to induce maximal transcription.
- the Stat6 signaling pathway may play a role in maintaining the Th1/Th2 cytokine balance by directly and indirectly down-regulating the production of proinflammatory cytokines
- Results demonstrate that induction of adenine nucleotide translocase 3 by interleukin-4 and interferon-gamma proceeds via pathways involving STAT6 and STAT1, respectively.
- STAT6 activation mediates a transcriptional enhancement of trefoil factor-3 (TFF3) by induction of de novo synthesized protein in mucus-producing HT-29 CL.16E intestinal goblet cells.
- Constitutive STAT6 phosphorylation and DNA-binding activity were detected in primary mediastinal large B-cell lymphoma cell lines but not diffuse large B-cell lymphoma cell lines
- IL-4 and IL-13 promote Stat6 serine phosphorylation in PHA-activated human T-cells.
- As no exonic variants of STAT6 are known as yet, repeat polymorphisms in the regulatory regions and their haplotypes could be important in deciphering the genetic role of STAT6 in asthma and atopy.
- FN-gamma regulates IL-4- and STAT6-dependent signaling and gene expression in airway epithelial cells by multiple mechanisms
- genetic variants within STAT6 contribute significantly to IgE regulation and manifestation of atopic diseases
- Role for Stat6 in apoptosis regulation. Stat6(null phenotype) cell lines exhibit variably increased levels of Th1 cytokines. May be source for investigations into Inflammatory bowel disease pathophysiology.
- IL-4 and IL-13 mediate the hypercontractility of intestinal muscle via a STAT6 pathway at the level of the smooth muscle cell. The STAT6 pathway may contribute to the hypercontractility of intestinal muscle in Crohn's disease.
- p100 has an important role in the assembly of STAT6 transcriptosome, and that p100 stimulates IL-4-dependent transcription by mediating interaction between STAT6 and CBP and recruiting chromatin modifying activities to STAT6-responsive promoters
- PI3-K promotes the expression of TFF3 and MUC2 and that the PI3-K pathway may play a pivotal role in intestinal goblet cell differentiation.
- Alterations in the STAT6 pathway may play a crucial role in the pathogenesis of distinct subgroups of patients with Crohn's disease.
- IL-4 regulates TNFalpha-induced IL-8 expression at a transcriptional level and this mechanism involves STAT6 and NF-kappaB transcription factors
- results demonstrate that epithelial eotaxin-3 is up-regulated in the context of a T helper 2 mediated inflammatory bowel disease via the signal transducer and activator of transcription 6
- Findings suggest that Stat6 signaling pathway plays a role in the regulation of cell proliferation and apoptosis in colon cancer cells, which promises further investigation for targeted cancer therapy.
- STAT6 binding to STAT6 promotor gene was regulated by H4 receptor-induced signal transduction and/or cross talk particularly in atopic human lymphocytes ex vivo
- IL-4 has differential effects in coronary artery smooth muscle cells: short-term exposure enhances OPG production through a STAT6-dependent mechanism, but long-term exposure causes Cbfa1-dependent osteogenic transformation and decreased production of OPG
- Essential for IL-4-induced human T-cell expression of CCL17/thymus- and activation-regulated chemokine(TARC).
- Activation of STAT6 appears to be a key factor in P-selectin expression induced by substance P and IL-4 because treatment with STAT6 decoy oligodeoxynucleotides significantly inhibited P-selectin expression.
- Stat6 exerts a stimulatory effect on early growth response (Egr)-1 gene and platelet-derived growth factor (PDGF) ligand mRNA transcription.
- The STAT6 G2964A polymorphism is not involved in the genetic susceptibility to ulcerative colitis in Chinese patients.
- specific increases in T-cell protein tyrosine phosphatase expression in activated-B-cell-like diffuse large B-cell lymphomas may contribute to the different biological characteristics of these tumors
- STAT6 may contribute to disease susceptibility in endometriosis
- Unphosphorylated STAT6 plays a novel role in the pathogenesis of non-small cell lung cancer.
- Collectively, these data suggest a link between the inducible phenotype of CCL23 expression in monocytes by the prototype Th2 molecule pair IL-4/STAT6 and the increased number of CCL23-expressing cells in skin of atopic dermatitis patients.
- Cross-talk between STAT6 and extracellular signal-regulated kinase (Erk) is the basis of the functional interaction between Jak/STAT and MAP kinase pathways activated by interleukin (IL)-4.
- No statistically significant difference was found in the distribution of the STAT-6 G2964A polymorphisms between asthmatic patients and controls.
- The transcription factor STAT6 may play a pivotal role in the activation of eotaxin transcription in response to IL-4.
- STAT6 overexpression detected in a classical Hodgkins lymphoma cell line
- In lymphocyte-predominant Hodgkin lymphoma SOCS1 function may thus be frequently impaired by mutations, and this may contribute to high JAK2 expression and activation of the JAK2/STAT6 pathway.
- STAT6 is a survival factor in prostate cancer regulating the genetic transcriptional program for prostate cancer progression.
- evidence provided that a distal tandem STAT6 element elevates expression from the CCL17 locus approximately twofold.
- activation induces osteoprogeterin expression in cooperation with IL-4 and IL-13
- A STAT6 gene polymorphism is associated with high infection levels in urinary schistosomiasis.
- These findings, together with the observation of constitutive Stat6 activation in many human malignancies, suggest that Stat6 activities could be a biomarker for cancer cell's invasive/metastatic capability.
- IL-13 has anti-angiogenic activity as a result of activation of JAK2 and subsequent activation of STAT6.
- Data show that IL-4-induced Stat6 activities affect apoptosis and gene expression in breast cancer cells.
- Data suggest that histamine receptor H4R-selective ligands influence the STAT6 transcription activation domain and DNA-binding.
- STAT6 plays pivotal roles on IL-13- and IL-4-induced apoptosis in vascular endothelial cells.
- Constitutively increased expression of Stat6 negative regulators SOCS-1 and SHP-1, together with decreased expression of positive regulator PP2A, may play a role in forming the inactive Stat6(null) phenotype in colon cancer
- analyzed IL-4 receptor expression, STAT-6 activation by IL-4, and STAT-6 inhibition by an anti-IL-4 antibody or by STAT-6 small-interfering RNA transfection
- IL-4 induces PTP1B mRNA expression in a phosphatidylinositol 3-kinase-dependent manner and enhances PTP1B protein stability to suppress IL-4-induced STAT6 signaling.