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Human SOCS3 ELISA Kit for Sandwich ELISA - ABIN414790
Zeitvogel, Dalpke, Eiz-Vesper, Kracht, Dittrich-Breiholz, Werfel, Wittmann: Human primary keratinocytes show restricted ability to up-regulate suppressor of cytokine signaling (SOCS)3 protein compared with autologous macrophages. in The Journal of biological chemistry 2012
Show all 3 Pubmed References
Human SOCS3 ELISA Kit for Sandwich ELISA - ABIN366182
Ostalska-Nowicka, Smiech, Jaroniec, Zaorska, Zawierucha, Szaflarski, Malinska, Nowicki: SOCS3 and SOCS5 mRNA expressions may predict initial steroid response in nephrotic syndrome children. in Folia histochemica et cytobiologica / Polish Academy of Sciences, Polish Histochemical and Cytochemical Society 2012
Mouse (Murine) SOCS3 ELISA Kit for Sandwich ELISA - ABIN425023
Speth, Bourdonnay, Penke, Mancuso, Moore, Weinberg, Peters-Golden: Alveolar Epithelial Cell-Derived Prostaglandin E2 Serves as a Request Signal for Macrophage Secretion of Suppressor of Cytokine Signaling 3 during Innate Inflammation. in Journal of immunology (Baltimore, Md. : 1950) 2016
we report the surprising finding that zebrafish respond to optic nerve lesion by inducing the expression of Sfpq and Socs3a
stat3 (show STAT3 ELISA Kits)/socs3 pathway is a key response in all tissue regeneration in zebrafish.
Trpm7 (show TRPM7 ELISA Kits) regulates exocrine pancreatic development via the Mg(2 (show MCOLN1 ELISA Kits)+)-sensitive Socs3a pathway.
SOCS3 expression in response to trauma is unaffected by blockade of the mitogen-activated protein kinase (show MAPK1 ELISA Kits) 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 (show SOCS1 ELISA Kits) and SOCS3 proteins.
Data suggest that SOCS3 is an important signaling protein in CLL, and Hsp90 (show HSP90 ELISA Kits) inhibitors represent an approach to target transcriptional repression in B cell lymphoproliferative disorders.
6-Hydroxy-3-O-methyl-kaempferol 6-O-glucopyranoside potentiated the inhibitory effect of IFN-alpha (show IFNA ELISA Kits) on hepatocellular carcinoma cell proliferation through activation of the JAK (show JAK3 ELISA Kits)/STAT (show STAT1 ELISA Kits) signaling pathway by inhibiting SOCS3 expression.
SOCS3 was down-regulated in CML cell lines and most of BMNCs from CML patients, and the expression level of SOCS3 was associated with the inhibition of cell proliferation and drug resistance of CML cells.
SOCS3 is involved in suppression of Helicobacter pylori induced STAT3 (show STAT3 ELISA Kits) phosphorylation by docosahexaenoic acid pretreatment.
The increased miR (show MLXIP ELISA Kits)-203 expression is associated with the reduced anti-inflammatory mediator SOCS-3 expression and the increased endothelial adhesion molecule (show NCAM1 ELISA Kits) expression in maternal vessel endothelium in preeclampsia.
Our results show, for the first time, that SOCS-3 regulates leptin (show LEP ELISA Kits)-induced responses in cartilage
Studies indicate that suppressors of cytokine signaling (SOCS (show CISH ELISA Kits)) proteins CIS (show CISH ELISA Kits), SOCS1 (show SOCS1 ELISA Kits), and SOCS3 can be considered the third immunocheckpoint molecules since they regulate cytokine signals that control the polarization of CD4 (show CD4 ELISA Kits)(+) T cells and the maturation of CD8 (show CD8A ELISA Kits)(+) T cells.
In M1-activated human monocyte-derived macrophages, SOCS3 silencing decreased expression of proinflammatory markers and increased M2 macrophage markers. SOCS3 knockdown radically affects the temporal dynamics of M1 macrophages' particle engulfment through increased PI3K and Ras-related C3 botulinum toxin substrate 1 (Rac1) activity. SOCS3 drives macrophage inflammatory responses and modulates key phagocytosis signaling.
The results of this study demonstrated that HBx of hepatitis B virus impairs interferon signaling via increased expression of SOCS3 and PP2A.
Overexpression of SOCS3 inhibited proliferation, migration, invasion and tumorigenic ability of colorectal cancer cells while increased cell apoptosis. Reduced expression of SOCS3 promoted the growth and metastasis of colorectal cancer.
SOCS3 is an important negative regulator of insulin (show INS ELISA Kits) signaling in porcine adipocytes.
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 (show IL10 ELISA Kits) and SOCS-3, which may have attenuated the capacity of mononuclear phagocytes to initiate inflammatory and adaptive immune responses.
Mechanistic analysis indicated that E47 (show TCF3 ELISA Kits) activated expression of the transcription factor Spi-B (show SPIB ELISA Kits) and the suppressor of cytokine signaling 3 (SOCS3), which both downregulated Foxp3 (show FOXP3 ELISA Kits) expression. These findings demonstrate that the balance of Id3 (show ID3 ELISA Kits) and E47 (show TCF3 ELISA Kits) controls the maintenance of Foxp3 (show FOXP3 ELISA Kits) expression in Treg cells and, thus, contributes to Treg cell plasticity.
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 (show RBL1 ELISA Kits), 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 (show MRPS12 ELISA Kits)) 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 (show JUN ELISA Kits) or early gene expression and/or viral tegument proteins in the early stimulation of SOCS1 (show SOCS1 ELISA Kits) and SOCS3 during murine cytomegalovirus infection.
oncostatin M (show OSM ELISA Kits) mitigated the proliferation of Th17 cells and decreased the expression of IL-17 (show IL17A ELISA Kits) and IL-21 (show IL21 ELISA Kits); it promoted the activation of suppressor of cytokine signaling 3 (SOCS3), STAT3 (show STAT3 ELISA Kits), and STAT5 (show STAT5A ELISA Kits); observations suggest that OSM (show OSM ELISA Kits) can inhibit Th17 differentiation by reciprocally controlling SOCS3, STAT3 (show STAT3 ELISA Kits), and STAT5 (show STAT5A ELISA Kits)
Results demonstrate a novel tunable form of cross-talk in which alveolar epithelial cells use Prostaglandin E2 (PGE2) as a signal to request SOCS3 from alveolar macrophages to dampen their endogenous inflammatory responses during infection.
Loss of SOCS3 significantly accelerated the pathology and inflammatory disease characteristic of SOCS1 (show SOCS1 ELISA Kits) deficiency. We propose a model in which SOCS1 (show SOCS1 ELISA Kits) and SOCS3 operate independently to control specific cytokine responses and together modulate the proliferation and activation of lymphoid and myeloid cells to prevent rapid inflammatory disease
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