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Validated All-in-One™ qPCR Primer for SOCS3(NM_003955.4) Search again
Product ID:
HQP088473
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ATOD4, CIS3, Cish3, SOCS-3, SSI-3, SSI3
Gene Description:
suppressor of cytokine signaling 3
Target Gene Accession:
NM_003955.4(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
This gene encodes a member of the STAT-induced STAT inhibitor (SSI), also known as suppressor of cytokine signaling (SOCS), family. SSI family members are cytokine-inducible negative regulators of cytokine signaling. The expression of this gene is induced by various cytokines, including IL6, IL10, and interferon (IFN)-gamma. The protein encoded by this gene can bind to JAK2 kinase, and inhibit the activity of JAK2 kinase. Studies of the mouse counterpart of this gene suggested the roles of this gene in the negative regulation of fetal liver hematopoiesis, and placental development. [provided by RefSeq].
Gene References into function
- active MKK6 in HepG2 cells enhanced basal activity or IL-6-induced transcriptional activation of a SOCS3 promoter
- evidence for pY429pY431 being a new high affinity binding site for SOCS-3 on the EpoR
- SOCS-3 is a major regulator of growth hormone signaling in insulin-producing cells
- chronic expression confers resistance to IFN-alpha in chronic myelogenous leukemia cells
- These data suggest, that there are two, largely distinct modes of negative regulation of gp130 activity, despite the fact that both SOCS3 and SHP2 are recruited to the same site within gp130.
- translational control plays an important role in stabilization and function of SOCS3
- SOCS-3 may have a role in IL-6-mediated insulin resistance in liver
- Results describe the cloning and characterization of the promoter region of the human SOCS-3 gene.
- Data showing that SOCS3 is not recruited to phosphotyrosine motifs of the IL-10 receptor complex suggest that IL-10 signaling is less sensitive than IL-6 signaling to inhibition by SOCS3.
- induction of SOCS3 by Leishmania donovani provides a potent inhibitory mechanism by which intracellular microorganisms may suppress macrophage activation and interfere with the host immune response
- SOCS-3 plays an important role in the suppression of cytokine signaling by GH in down-regulating the acute phase response after injury.
- acceleration of degradation by tyrosine phosphorylation
- These data indicate that SOCS-3 has an important role in regulating the onset and maintenance of T(H)2-mediated allergic immune disease.
- hypermethylation in CpG islands of the functional SOCS-3 promoter that correlates with its transcription silencing in primary lung cancer tissue samples
- rapidly induced in amnion FL cells in HSV-1 infection and appears to be mainly responsible for suppression of IFN signaling and IFN production during the HSV-1 infection.
- Frequent hypermethylation of the functional SOCS-3 promoter correlates with its transcription silencing in NSCLC cell lines and primary lung cancer tissue samples; methylation silencing of SOCS-3 may be used as a marker for early detection of NSCLC
- Our results demonstrate that SOCS-1 and SOCS-3 proteins inhibit IFN-alpha-induced activation of the Jak-STAT pathway and expression of the antiviral proteins 2',5'-OAS and MxA.
- Homozygosity for the A-allele of the C -920-->A promoter polymorphism of the SOCS3 gene may be associated with increased whole-body insulin sensitivity.
- Leptin resembles immune molecules called cytokines, which another protein, Socs3, inhibits. Colleagues wondered whether Socs3 also suppresses leptin and promotes resistance to the hormone.
- interleukin-1beta regulates interleukin-6-induced suppressor of cytokine signaling 3 expression
- SOCS-3 expression in human skeletal muscle in vivo is not related to insulin resistance in the presence of elevated IL-6 concentrations suggesting that cytokine action could differ in type 2 diabetic patients and nondiabetic obese subjects.
- SOCS1 and SOCS2 but not SOCS3 suppressed the growth of ovarian and breast cancer cells.
- overexpression of suppressor of cytokine signaling 3 is associated with anaplastic large cell lymphoma
- The insertion of amino acid exchanges into the kinase inhibitory regions of SOCS-3 demonstrated a requirement of these domains for a proper inhibitory function.
- The SOCS3 mRNA expression in bone marrow cells from CML patients who responded well to IFN-alpha therapy was significantly lower than that in cells from healthy volunteers and patients who were resistant to IFN-alpha therapy.
- SOCS-3 is not a tumour suppressor but rather a protector of tumour cells.
- SOCS3/CIS3 regulates hepatocyte growth factor-induced keratinocyte migration by inhibiting signal transducer and activator of transcription 3 phosphorylation
- The induction of SOCS3 by HSV-1 occurs via STAT3 activation immediately after HSV-1 infection.
- promoter methylation and subsequent transcript downregulation of SOCS-3 transcripts and, to a much lesser extent, SOCS-1 are involved in the multistep carcinogenesis of head and neck squamous cell carcinoma
- loss of SOCS-3 by the associated DNA methylation confers cells advantage in growth and migration
- estrogen receptor 1 directly regulates human SOCS-3 promoter activity in human breast cancer cells
- Inhibition of function in dominant-negative SOCS3 transgenic mice clearly reduces the severity of allergic conjunctivitis
- this study suggests a potential novel function of SOCS-3 in regulating keratinocyte proliferation and differentiation in vitro and during skin repair in vivo.
- Results suggest a novel interaction between the SOCS1 and SOCS3 proteins and the FGFR3 signaling pathway.
- SOCS-3 inhibits IL-1 signal transduction by inhibiting ubiquitination of TRAF6, thus preventing association and activation of TAK1.
- Able to repress the activity of the Brk non-receptor tyrosine kinase.
- role for IL-11 via pSTAT3 and SOCS3 in initiating and progressing decidualization
- Our data also show that SOCS3 promoted maintenance of neural stem cells
- Data demonstrate that SOCS3 inhibits leptin activation of AMPK and suggest this impairment of leptin signaling in skeletal muscle may contribute to the aberrant regulation of fatty acid metabolism observed in obesity.
- Deletion of the SOCS3 gene in hepatocytes promotes the activation of STAT3, resistance to apoptosis, and an acceleration of proliferation, resulting in enhanced hepatitis-induced hepatocarcinogenesis.
- These data argue for the existence of a novel cAMP/Epac/Rap1/SOCS-3 pathway for limiting IL-6 receptor signaling in Endothelial Cells and illuminate a new mechanism by which cAMP may mediate its potent anti-inflammatory effects.
- Decreased SOCS3 expression in obese adipose tissue may reflect a defective leptin signaling pathway.
- The increase in mRNA for SOCS-3, which correlates with elevated levels of SOCS protein and positive immunostaining in M. avium/HIV-1 co-infected tissues.
- elevated expression of SOCS genes is a specific lesion of breast-cancer cells that may confer resistance to proinflammatory cytokines and trophic factors, by shutting down STAT1/STAT5 signaling that mediate essential functions in the mammary gland
- SOCS3 binds the phosphorylated immunoreceptor tyrosine-based inhibitory motif (ITIM) of sialic acid-binding immunoglobulin-like lectin (siglec) 7 and targets it for proteasomal-mediated degradation.
- Collectively, our results show that SOCS-3 antagonizes regulation of cellular events by cAMP and is expressed in human prostate cancer.
- SOCS-3 epigenetic silencing is responsible for sustained IL-6/STAT-3 signaling and enhanced Mcl-1 expression in cholangiocarcinoma
- Using RT-PCR, we demonstrated for the first time that neutrophils express mRNA for SOCS-3. It is interesting that IL-4 increased expression of SOCS-3 at the mRNA and protein levels.
- inactivation of the SOCS3 gene by hypermethylation may be involved in the promotion of malignant behavior of melanomas
- SOCS3 overexpression reduced proliferation.
- a defect in expression of SOCS-2 and SOCS-3 genes may be crucial for the IGF-I hypersensitivity and progressive increase in erythroid cell population size characteristic of Polycythemia vera.
- This is the first demonstration of SOCS-mediated ubiquitination and routing of a cytokine receptor and its impact on maintaining an appropriate signaling output.
- SOCS3 may possibly play a role in IL-6 resistance in at least a fraction of tumors.
- Altered SOCS gene expression leads to increased cell signaling through the ERK-MAPK pathway and may play a role in disease pathogenesis by enhancing glioblastoma multiforme radioresistance.
- our data do not suggest evidence for a major role of the respective SNPs in SOCS3 in the pathogenesis of extreme obesity in our study groups
- Interleukin-6 (IL-6) was expressed in monocytes and B cells, IL-10 in monocytes, and suppressor of cytokine signaling 3 in monocytes and T cells from patients with active disease.
- Increased expression of mucosal SOCS3, but not of SOCS1, may play a critical role in the development of the colonic inflammation of ulcerative colitis.
- This study details a novel mechanism of SOCS3 up-regulation by PGE2 in breast cancer cells that appears to be STAT independent and involve Sp1 binding to the promoter.
- SOCS3 expression may influence the response to antiviral therapy and genotype 1b hepatitis C virus might induce its up-regulation. This may account for the different responses to therapy between genotype 1-infected and genotype 2-infected patients.
- SOCS3 remained significantly unchanged in polycystic ovarian syndrome women
- The infection of cells with adenovirus CN305 (AdCN305)-SOCS3 and AdCN305-cpp-SOCS3 resulted in dramatic cytotoxicity in liver tumor cells.
- SOCS-3 inhibits androgen-stimulated proliferation by influencing cell cycle regulation in a prostate cancer cell line.
- We conclude that endogenous SOCS3 inhibits AP-1 activity through blocking of JNK phosphorylation.
- Reduced expression of SOCS-3 is closely related to lymph node metastasis. Therefore, SOCS-3 may be a good predictor for lymph node metastasis.
- Human sarcopenia reveals an increase in SOCS-3 and myostatin and a reduced efficiency of Akt phosphorylation.
- SOCS3 and SOCS1 critically regulate influenza A virus-triggered innate immune responses by inhibiting type I interferon alphabeta receptor (IFNAR)1 antiviral signaling and differentially modulating inflammatory signaling pathways.
- The methylation status of CpG islands of SOCS3 genes in chronic myeloproliferative neoplasms.
- SOCS3 negatively regulates cell motility and decreased SOCS3 induced by methylation may confer a migration advantage to A549 cells. This suggest a negative role of SOCS3 in PYK2 signaling: previously unidentified regulatory mechanism for PYK2 function.
- the lymphadenitis due to M. tuberculosis was associated with activated lysozymes and SOCS-3 but not SOCS-1 compared to controls, which may play a role in the long-term bacterial replication and altered immune modulation characteristic of the disease.
- Oncostatin M stimulation of astrocytes leads to induction of SOCS-3 expression and activation of ERK1/2 and JNK pathways.
- monocyte SOCS3 correlated with glomerular filtration rate, urea and diastolic blood pressure
- SOCS-3 acts as a negative regulator of the cell cycle progression under E2F/DP-1 control by interfering with heterodimer formation between DP-1 and E2F
- Constitutive and altered SOCS-3 expression may have potential roles in a subset of hepatocellular carcinoma patients.
- The methylation of SOCS3 may be involved in the pathogenesis of glioblastoma multiforme and in the resistance of this neoplasm to conventional treatment.
- SOCS3 promoter methylation iss detected in 32% of patients with idiopathic myelofibrosis suggesting a role for SOCS3 methylation in this disorder.
- difference in SOCS1, SOCS2 and SOCS3 transcript levels between normal individuals and SLE patients is not statistically significant
- SOCS3 expression in skeletal muscle is not up-regulated in women, despite very high serum leptin concentrations compared to men
- SOCS3 negatively regulates IL-1beta-induced MUC8 gene expression.
- CCL11 induces SOCS1 and SOCS3 expression in murine macrophages, human monocytes, and dendritic cells and inhibits GM-CSF-mediated STAT5 activation and IL-4-induced STAT6 activation in a range of hematopoietic cells.
- increased ratio of sgp130/sIL-6R production and/or reduced sIL-6R production combined with down-regulation of IL-6R and SOCS-3 expression in trophoblasts may lead to less cytokine inhibitory activity in preeclampsia placentas
- influenza A viruses not only suppress IFNbeta gene induction but also inhibit type I IFN signaling through a mechanism involving induction of the SOCS-3 protein
- These results suggest that the interaction of SOCS3 with MAP1S and the integrity of the microtubule cytoskeleton play an important role in the negative regulation of SOCS3 on IL-6 signaling.
- Enhanced SOCS-3 gene expression could promote IL-10 production by placental trophoblast cells, suggesting that SOCS-3 may play an important role in regulation of cytokine induced anti-inflammatory response in placental trophoblasts.
- There is no strong effect of the common genetic variation within the SOCS3 gene on the development of type 2 diabetes mellitus.
- SOCS3 genetic variants play a role in human obesity.
- SOCS3 is a tumor suppressor in breast cancer cells that is regulated by PRL