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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 (show STAT3 Proteins)/socs3 pathway is a key response in all tissue regeneration in zebrafish.
Trpm7 (show TRPM7 Proteins) regulates exocrine pancreatic development via the Mg(2 (show MCOLN1 Proteins)+)-sensitive Socs3a pathway.
SOCS3 expression in response to trauma is unaffected by blockade of the mitogen-activated protein kinase (show MAPK1 Proteins) 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 Proteins) and SOCS3 proteins.
Our results show, for the first time, that SOCS-3 regulates leptin (show LEP Proteins)-induced responses in cartilage
Studies indicate that suppressors of cytokine signaling (SOCS (show CISH Proteins)) proteins CIS (show CISH Proteins), SOCS1 (show SOCS1 Proteins), and SOCS3 can be considered the third immunocheckpoint molecules since they regulate cytokine signals that control the polarization of CD4 (show CD4 Proteins)(+) T cells and the maturation of CD8 (show CD8A Proteins)(+) 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 (show IFNA Proteins) signaling via increased expression of SOCS3 and PP2A (show PPP2R4 Proteins).
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, which is a critical negative regulator of cytokine response to tuberculosis infection and its nearby lncRNA XLOC_012582, were highly expressed in active tuberculosis B cells.
Data show that the suppressor of cytokine signaling-3 (SOCS3) promoter hypermethylation was associated with relatively low mRNA expression in tumor tissues.
Data show that ELOVL7, SOCS3, ACSL4 (show ACSL4 Proteins) and CLU (show CLU Proteins) were upregulated while PRKAR1A (show PRKAR1A Proteins) and ABCG1 (show ABCG1 Proteins) were downregulated in the phlegm-dampness group.
There are pronounced changes in the expression of SOCS3 only in Non-allergic Asthma.
epigenetic signatures at AQP3 (show AQP3 Proteins) and SOCS3 engage in low-grade inflammation across different tissues, possible via JAK (show JAK3 Proteins)/STAT (show STAT1 Proteins) mediated pathways
SOCS3 is an important negative regulator of insulin (show INS Proteins) 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 Proteins) and SOCS-3, which may have attenuated the capacity of mononuclear phagocytes to initiate inflammatory and adaptive immune responses.
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 Proteins), 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 Proteins)) 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 Proteins) or early gene expression and/or viral tegument proteins in the early stimulation of SOCS1 (show SOCS1 Proteins) and SOCS3 during murine cytomegalovirus infection.
oncostatin M (show OSM Proteins) mitigated the proliferation of Th17 cells and decreased the expression of IL-17 (show IL17A Proteins) and IL-21 (show IL21 Proteins); it promoted the activation of suppressor of cytokine signaling 3 (SOCS3), STAT3 (show STAT3 Proteins), and STAT5 (show STAT5A Proteins); observations suggest that OSM (show OSM Proteins) can inhibit Th17 differentiation by reciprocally controlling SOCS3, STAT3 (show STAT3 Proteins), and STAT5 (show STAT5A Proteins)
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 Proteins) deficiency. We propose a model in which SOCS1 (show SOCS1 Proteins) 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 study showed that leptin (show LEP Proteins) resistant infertility is caused in part by the leptin (show LEP Proteins) signaling molecule SOCS3. Deletion of SOCS3 from brain neurons delays the onset of diet-induced infertility.
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