Anti-SOCS3 monoclonal antibody, clone 26G0

Name: Anti-SOCS3 monoclonal antibody, clone 26G0
SKU: DCABH-1028
Rating: 5 (1 reviews)

Mouse anti-Human SOCS3 monoclonal antibody for WB, IHC-P

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG

Clone

26G0

Species Reactivity

Human

Immunogen

Recombinant full length Human SOCS3 produced in HEK293T cells (NP_003946).

Conjugate

Unconjugated

Applications

Application Notes

WB: 1/2000; IHC-P: 1/150;

Target

Alternative Names

SOCS3; suppressor of cytokine signaling 3; CIS3; Cish3; SOCS 3; SSI 3; CIS-3; STAT-induced STAT inhibitor 3; cytokine-induced SH2 protein 3; cytokine-inducible SH2 protein 3; SSI3; ATOD4; SSI-3; SOCS-3; MGC71791;

Entrez Gene ID

9021

UniProt ID

O14543

Product Background

Antigen Description

SOCS family proteins form part of a classical negative feedback system that regulates cytokine signal transduction. SOCS3 is involved in negative regulation of cytokines that signal through the JAK/STAT pathway. Inhibits cytokine signal transduction by binding to tyrosine kinase receptors including gp130, LIF, erythropoietin, insulin, IL12, GCSF and leptin receptors. Binding to JAK2 inhibits its kinase activity. Suppresses fetal liver erythropoiesis. Regulates onset and maintenance of allergic responses mediated by T-helper type 2 cells. Regulates IL-6 signaling in vivo (By similarity). Probable substrate recognition component of a SCF-like ECS (Elongin BC-CUL2/5-SOCS-box protein) E3 ubiquitin-protein ligase complex which mediates the ubiquitination and subsequent proteasomal degradation of target proteins. Seems to recognize IL6ST.

Pathway

ATF-2 transcription factor network, organism-specific biosystem; Adaptive Immune System, organism-specific biosystem; Adipocytokine signaling pathway, organism-specific biosystem; Adipocytokine signaling pathway, conserved biosystem; Adipogenesis, organism-specific biosystem; Antigen processing: Ubiquitination & Proteasome degradation, organism-specific biosystem;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

AlteredSOCS3DNA methylation within exon 2 is associated with increased mRNA expression in visceral adipose tissue in gestational diabetes

EPIGENETICS

Authors: Rancourt, Rebecca C.; Ott, Raffael; Schellong, Karen; Ziska, Thomas; Melchior, Kerstin; Henrich, Wolfgang; Plagemann, Andreas

Abstract

Overweight/obesity is the main risk factor for gestational diabetes mellitus (GDM). In our cohort of pregnant women with GDM, n = 19, and without, n = 22, we previously reported a significant increase inSOCS3mRNA expression (+62%) in visceral adipose tissue (VAT) according to GDM, without altered promoter DNA-methylation. Here, we examined methylation status of additionalSOCS3exon 2 regions in VAT and maternal blood. We found significantly altered methylation at specific CpG sites corresponding to aberrant mRNA expression levels ofSOCS3in VAT. We propose a potential regulatory element/region within exon 2; however, this region does not appear to be a good blood-marker representing VAT.

MicroRNA-19a-3p promotes rheumatoid arthritis fibroblast-like synoviocytes via targeting SOCS3

JOURNAL OF CELLULAR BIOCHEMISTRY

Authors: Chen, Yiyue; Wang, Wanchun; Chen, You; Tang, Qi; Zhu, Weihong; Li, Ding; Liao, Lele

Abstract

Rheumatoid arthritis (RA) is a common chronic autoimmune disease and effective treatment for RA is still lacking. In this study, the regulatory role of miR-19a-3p in RA was investigated. Quantitative polymerase chain reaction analysis of human blood samples showed that the level of miR-19a-3p was significantly lower in the RA patients compared with that in healthy patients (P<0.05). In RA fibroblast-like synoviocytes (RAFLS), miR-19a-3p and suppressor of cytokine signaling 3 (SOCS3) were also downregulated and upregulated, respectively, compared with those of normal FLS. Transfection of miR-19a-3p mimic in RAFLS inhibited cell proliferation and promoted cell apoptosis. TargetScan identified SOCS3 as a target of miR-19a-3p, which was confirmed by dual-luciferase assay. Western blot indicated that SOCS3 protein level was significantly decreased after miR-19a-3p overexpression. Moreover, SOCS3 silencing through siRNA transfection also enhanced cell proliferation, meanwhile inhibiting RAFLS apoptosis. In addition, SOCS3 overexpression abrogated the effects of miR-19a-3p overexpression on cell proliferation and apoptosis, corroborating that SOCS3 acts as a downstream effector in the miR-19a-3p-mediated function of RAFLS. These findings suggest that miR-19a-3p plays an important role in RA, and the miR-19a-3p/SOCS3 axis may become a potential therapeutic target for RA.