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Human SOCS3 Protein expressed in Wheat germ - ABIN1320930
Jiang, Biswas, Steinle: Serine 307 on insulin receptor substrate 1 is required for SOCS3 and TNF-? signaling in the rMC-1 cell line. in Molecular vision 2014
we report the surprising finding that zebrafish respond to optic nerve lesion by inducing the expression of Sfpq and Socs3a
stat3/socs3 pathway is a key response in all tissue regeneration in zebrafish.
Trpm7 regulates exocrine pancreatic development via the Mg(2+)-sensitive Socs3a pathway.
SOCS3 expression in response to trauma is unaffected by blockade of the mitogen-activated protein kinase pathway by chemical inhibitors
The suppressor of cytokine signaling 3 gene was identified in this species, and the base sequence and deduced amino acid sequence are presented.
in homozygotes, GH signaling is reduced by the action of the SOCS1 and SOCS3 proteins.
SOCS1/3-mediated degradation of IFN regulatory factor 7 directly regulates TLR7 signaling and type I IFN production in pDCs.
The expression of SOCS3 in peripheral blood mononuclear cells and liver tissues of non-responding CHB[ chronic hepatitis B] patients was significantly higher than that of responding CHB patients during interferon and nucleoside antiviral therapy. We speculated that SOCS3 might affect the antiviral efficacy through negative regulation of JAK-STAT signaling pathway, and partly expose the mechanism of interferon resistance.
TGF-beta1 can downregulate the mRNA expression of SOCS-3 and upregulate the mRNA expression of SREBP-1c.
SOCS3 is highly tyrosine phosphorylated by c-Abl and that tyrosine phosphorylation of SOCS3 is required for the survival and tumorigenesis of certain cells. Our findings provide novel insights into complicated mechanisms underlying the oncogenic function of Abl kinases.
In vitro significance of SOCS-3 and SOCS-4 and potential mechanistic links to wound healing have been presented.
Loss or reduced levels of SOCS3 have been linked to cancer-associated inflammation and suppressive immunity leading to enhanced breast tumor growth lung metastasis.
BORIS plays a role in epigenetic regulation of SOCS3 gene promoter methylation and histone methylation in hepatocellular carcinoma.
Downregulation of miR-340 inhibited GC cell proliferation, arrested cell cycle, and facilitated apoptosis through upregulating SOCS3 expression to suppress JAK-STAT3 signaling pathway.
Low SOCS3 expression is associated with higher grade breast cancer.
Low SOCS3 expression is associated with invasion and lymph node metastasis in gastric cancer.
Results show the CAT haplotype in SOCS3 was associated with metabolic syndrome (MetS) in Mexican Mestizos, and type 2 diabetes in Mexican Amerindians.
SOCS3 overexpression decreased JAK-STAT3 signaling pathway activity, declined Bcl-2 expression, inhibited cell proliferation, elevated cell apoptosis, and enhanced Adriamycin sensitivity in T24 cells
miR203 expression may be upregulated by IL17 stimulation, and miR203 is a positive regulator of IL17induced VEGF secretion.
SOCS3 DNA methylation is associated with body weight and moderates the effect of cumulative stress on obesity.
polymorphisms associated with risk of head and neck squamous cancer
SOCS3 was targeted by miR30a- 5p in allergic rhinitis
Cellular viability was significantly decreased, whereas IL6 and TNFalpha levels were significantly increased, following High Glucose stimulation of A549 cells. In addition, the protein levels of SOCS3, pJAK2 and pSTAT3 were significantly increased in High Glucosetreated cells.
this study shows that Nrf2 activation induces lipocyte phenotype in hepatic stellate cells via enhancing SOCS3-dependent feedback inhibition on JAK2/STAT3 cascade
SOCS-1, SOCS-2, and SOCS-3 proteins may directly or indirectly, have important roles in development and pathogenesis of papillary thyroid cancer
Our study showed that the expressions of HER2, STAT3, and SOCS3 are associated with the progression of ovarian cancer (OC), and higher expressions of HER2 and STAT3 and lower expression of SOCS3 predict poor prognosis of OC.
In porcine circovirus type 2 subclinical infection, SOCS3 interacted with STAT3 and TNF receptor-associated factor 2, suggesting mechanisms by which SOCS3 inhibits IL-6 and TNF-alpha signaling.
SOCS3 is an important negative regulator of insulin signaling in porcine adipocytes.
mapping to chromosome 12
Low SOCS3 expression is required for milk synthesis and proliferation of dairy cow mammary epithelial cells in vitro.
Monocytes obtained from cows with subclinical infection with MAP had upregulated expression of IL-10 and SOCS-3, which may have attenuated the capacity of mononuclear phagocytes to initiate inflammatory and adaptive immune responses.
SOCS3 critically controls the phenotype and function of macrophages and neutrophils under inflammatory conditions and loss of SOCS3 promotes the angiogenic phenotype of the cells through up-regulation of arginase-1.
SOCS3 impacts on IEC turnover following T. muris infection, potentially through enhancement of IDO. IDO may dampen the immune response which can drive intestinal epithelial cell hyperproliferation in the absence of SOCS3, demonstrating the intricate interplay of immune signals regulating mucosal homeostasis, and suggesting a novel tumour suppressor role of SOCS3.
The findings of this indicated that co-deletion of PTEN and SOCS3 results in modest but measureable enhancement of early regeneration of DRG axons following crush injury.
Our findings suggest a role for murine cytomegalovirus (MCMV)-related stimulation of SOCS1 and SOCS3 in the progression of retinal disease during ocular, but not systemic, MCMV infection.
Lentivirusmediated overexpression of SOCS3 was revealed to ameliorate neutrophilic airway inflammation by inhibiting pulmonary Th17 responses in mice with chronic Pseudomonas aeruginosa lung infections.
These data demonstrate that loss of SOCS3 in cardiomyocytes promotes deoxycorticosterone-acetate -salt-induced cardiac remodeling and inflammation.
In the present study, we investigated the hypothesis that SOCS3 expression in the VMH could exert an important role regulating the metabolic changes typically observed during pregnancy and lactation.
SOCS3 was upregulated in lung CD4+ T cells in a mouse model of chronic PA lung infection and exogenous SOCS3 suppressed Th17-mediated neutrophil recruitment in vitro.
findings show SOCS3 does not appear to mediate the early inflammatory or leucine-induced changes in protein synthesis in skeletal muscle
The strength of long bones is determined by coalescence of trabeculae during corticalization.This process is regulated by SOCS3 via a mechanism dependent on IL-6 and expression of sex hormones.
High SOCS3 expression is associated with glioma.
Mechanistic analysis indicated that E47 activated expression of the transcription factor Spi-B and the suppressor of cytokine signaling 3 (SOCS3), which both downregulated Foxp3 expression. These findings demonstrate that the balance of Id3 and E47 controls the maintenance of Foxp3 expression in Treg cells and, thus, contributes to Treg cell plasticity.
Our results show, for the first time, that SOCS-3 regulates leptin-induced responses in cartilage
Loss of suppressor of cytokine (SOCS3) expression in mature muscle fibers increased the inflammatory response to myotoxic injury but did not impair muscle regeneration in either adult or old mice. Therefore, reduced SOCS3 expression in muscle fibers is unlikely to underlie impaired muscle regeneration.
Findings revealed a novel participation of SOCS3 regulating several endocrine and metabolic aspects.
Findings indicate that inactivation of the Rb family proteins (Rb, p107, and p130) in hematopoietic stem cells (HSCs) progressively impairs their homeostasis, which is rescued upon repression of suppressor of cytokine signaling 3 protein (Socs3) expression in triple knockout (TKO) HSCs.
Data suggest that, in B cell lymphoma, expression of MIRN30 is up-regulated in both granulocytic myeloid-derived suppressor cells and monocytic myeloid-derived suppressor cells; in B cell lymphoma, 3prime untranslated region of Socs3 appears to be direct target of MIRN30 in myeloid-derived suppressor cell differentiation. (MIRN30 = microRNA 30; Socs3 = suppressor of cytokine signaling 3 protein)
Cell type-specific, different roles for viral immediate early or early gene expression and/or viral tegument proteins in the early stimulation of SOCS1 and SOCS3 during murine cytomegalovirus infection.
oncostatin M mitigated the proliferation of Th17 cells and decreased the expression of IL-17 and IL-21; it promoted the activation of suppressor of cytokine signaling 3 (SOCS3), STAT3, and STAT5; observations suggest that OSM can inhibit Th17 differentiation by reciprocally controlling SOCS3, STAT3, and STAT5
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.
suppressor of cytokine signaling 3
, suppressor of cytokine signaling 3a
, STAT-induced STAT inhibitor 3
, cytokine-inducible SH2 protein 3
, cytokine signaling suppressor
, E2a-Pbx1 target gene in fibroblasts 10
, cytokine inducible SH2-containing protein 3
, suppressors of cytokine signaling 3