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anti-Human SOCS3 Antibodies:
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Human Polyclonal SOCS3 Primary Antibody for ELISA, IF (p) - ABIN670416
Liu, Ao, Zhou, Cui, Zhou, Yuan, Xiang, Cao, Liu: CpG island hypermethylation of multiple tumor suppressor genes associated with loss of their protein expression during rat lung carcinogenesis induced by 3-methylcholanthrene and diethylnitrosamine. in Biochemical and biophysical research communications 2010
Show all 4 Pubmed References
Human Monoclonal SOCS3 Primary Antibody for ELISA, WB - ABIN2476543
Rychlíková, Démant: Influence of non-H-2 genotype on the response to H-2-linked mixed lymphocyte reaction stimulating (MLR-S) genes. in Folia biologica 1975
Show all 4 Pubmed References
Human Polyclonal SOCS3 Primary Antibody for IHC, IHC (p) - ABIN4355049
Harris, Apolzan: Hexosamine biosynthetic pathway activity in leptin resistant sucrose-drinking rats. in Physiology & behavior 2014
Show all 2 Pubmed References
Human Monoclonal SOCS3 Primary Antibody for WB - ABIN153119
Xiang, Dong, Liu, Wang, Shi, Wei, Hu, Gong: Inhibitory effects of suppressor of cytokine signaling 3 on inflammatory cytokine expression and migration and proliferation of IL-6/IFN-?-induced vascular smooth muscle cells. in Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban 2013
Human Polyclonal SOCS3 Primary Antibody for ELISA, WB - ABIN262251
Roberts, Robb, Rakar, Hartley, Cluse, Nicola, Metcalf, Hilton, Alexander: Placental defects and embryonic lethality in mice lacking suppressor of cytokine signaling 3. in Proceedings of the National Academy of Sciences of the United States of America 2001
Human Polyclonal SOCS3 Primary Antibody for WB - ABIN1883384
Kim, Kim, Liu, Cao, Chen: Regulation of interleukin-6-induced hepatic insulin resistance by mammalian target of rapamycin through the STAT3-SOCS3 pathway. in The Journal of biological chemistry 2008
Human Monoclonal SOCS3 Primary Antibody for IF, IHC (p) - ABIN522456
Pierconti, Martini, Pinto, Cenci, Capodimonti, Calarco, Bassi, Larocca: Epigenetic silencing of SOCS3 identifies a subset of prostate cancer with an aggressive behavior. in The Prostate 2011
Human Monoclonal SOCS3 Primary Antibody for WB - ABIN94467
Neuwirt, Puhr, Cavarretta, Mitterberger, Hobisch, Culig: Suppressor of cytokine signalling-3 is up-regulated by androgen in prostate cancer cell lines and inhibits androgen-mediated proliferation and secretion. in Endocrine-related cancer 2007
Show all 4 Pubmed References
Human Polyclonal SOCS3 Primary Antibody for IHC, ELISA - ABIN1585262
van de Loo, Veenbergen, van den Brand, Bennink, Blaney-Davidson, Arntz, van Beuningen, van der Kraan, van den Berg: Enhanced suppressor of cytokine signaling 3 in arthritic cartilage dysregulates human chondrocyte function. in Arthritis and rheumatism 2012
we report the surprising finding that zebrafish respond to optic nerve lesion by inducing the expression of Sfpq (show SFPQ Antibodies) and Socs3a
stat3 (show STAT3 Antibodies)/socs3 pathway is a key response in all tissue regeneration in zebrafish.
Trpm7 (show TRPM7 Antibodies) regulates exocrine pancreatic development via the Mg(2 (show MCOLN1 Antibodies)+)-sensitive Socs3a pathway.
SOCS3 expression in response to trauma is unaffected by blockade of the mitogen-activated protein kinase (show MAPK1 Antibodies) 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 Antibodies) and SOCS3 proteins.
Our results show, for the first time, that SOCS-3 regulates leptin (show LEP Antibodies)-induced responses in cartilage
Studies indicate that suppressors of cytokine signaling (SOCS (show CISH Antibodies)) proteins CIS (show CISH Antibodies), SOCS1 (show SOCS1 Antibodies), and SOCS3 can be considered the third immunocheckpoint molecules since they regulate cytokine signals that control the polarization of CD4 (show CD4 Antibodies)(+) T cells and the maturation of CD8 (show CD8A Antibodies)(+) 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 Antibodies) signaling via increased expression of SOCS3 and PP2A (show PPP2R4 Antibodies).
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 (show ELOVL7 Antibodies), SOCS3, ACSL4 (show ACSL4 Antibodies) and CLU (show CLU Antibodies) were upregulated while PRKAR1A (show PRKAR1A Antibodies) and ABCG1 (show ABCG1 Antibodies) 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 Antibodies) and SOCS3 engage in low-grade inflammation across different tissues, possible via JAK (show JAK3 Antibodies)/STAT (show STAT1 Antibodies) mediated pathways
SOCS3 is an important negative regulator of insulin (show INS Antibodies) 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 Antibodies) 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 Antibodies), 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 Antibodies)) 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 Antibodies) or early gene expression and/or viral tegument proteins in the early stimulation of SOCS1 (show SOCS1 Antibodies) and SOCS3 during murine cytomegalovirus infection.
oncostatin M (show OSM Antibodies) mitigated the proliferation of Th17 cells and decreased the expression of IL-17 (show IL17A Antibodies) and IL-21 (show IL21 Antibodies); it promoted the activation of suppressor of cytokine signaling 3 (SOCS3), STAT3 (show STAT3 Antibodies), and STAT5 (show STAT5A Antibodies); observations suggest that OSM (show OSM Antibodies) can inhibit Th17 differentiation by reciprocally controlling SOCS3, STAT3 (show STAT3 Antibodies), and STAT5 (show STAT5A Antibodies)
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 Antibodies) deficiency. We propose a model in which SOCS1 (show SOCS1 Antibodies) 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 Antibodies) resistant infertility is caused in part by the leptin (show LEP Antibodies) 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