Ask about this productRelated genes to: SOCS3 antibody
- Gene:
- SOCS3 NIH gene
- Name:
- suppressor of cytokine signaling 3
- Previous symbol:
- -
- Synonyms:
- SSI-3, CIS3, SOCS-3, Cish3
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-13
- Date modifiied:
- 2019-04-23
Related products to: SOCS3 antibody
Related articles to: SOCS3 antibody
- Ulcerative colitis (UC) is a chronic inflammatory disorder associated with cytokine imbalance, epigenetic alterations, and metabolic-redox dysfunction. Despite the widespread use of mesalazine (5-ASA), therapeutic limitations remain. Norcantharidin (NCTD), a synthetic cantharidin analogue, may provide multi-target protection against UC. Experimental colitis was induced in male Sprague-Dawley rats by intrarectal administration of 4% acetic acid (AA). Rats received oral NCTD (10 mg/kg), 5-ASA (100 mg/kg), or their combination for 8 days. Disease severity was assessed by disease activity index, body weight, colon length, colon weight/length ratio, and histopathology. Colonic biomarkers were evaluated using ELISA, qRT-PCR, Western blotting, and immunohistochemistry. Fe and malondialdehyde (MDA) were measured as indicators of iron accumulation and lipid peroxidation. Molecular docking suggested that NCTD may adopt plausible binding poses within the binding pockets of AMPK, SIRT1, and DNMT1, providing structural support for potential protein-ligand interactions. NCTD significantly ameliorated AA-induced colitis, improving clinical and histological outcomes. These effects were associated with reduced IL-6, TNF-α, DNMT1, Fe, and MDA levels, restoration of SOCS3, activation of p-AMPK/SIRT1/FOXO3a signaling, and enhancement of Nrf2/HO-1 defenses. Combined NCTD/5-ASA treatment produced greater clinical and histological protection, with differential effects on molecular markers. Docking studies suggested favorable interactions of NCTD with AMPK, SIRT1, and DNMT1. NCTD treatment was associated with protection against experimental colitis, linked to modulation of inflammatory, epigenetic, metabolic, and antioxidant pathways. - Source: PubMed
Publication date: 2026/07/26
Yousef Eman HHawas Samia SSalama Mohamed MMetawee Mostafa ESakr Hader IAlarfaj Sumaiah JAlzokaky Amany A - Helicobacter pylori (H. pylori) is a major cause of chronic gastritis and gastric cancer. Macrophages are key regulators of gastric immunity, yet the mechanisms by which H. pylori reprogram macrophage activation and suppresses host immune responses remain unclear. RAW264.7 macrophages were infected with H. pylori PMSS1. Macrophage polarization, cytokine secretion, and JAK3/STAT5-SOCS3 signaling were examined by qRT-PCR, Western blotting, flow cytometry, and ELISA. Ritlecitinib was used to inhibit JAK3. Primary naive CD4⁺ T cells were treated with macrophage-conditioned medium to assess proliferation, CD25/CD69 activation, and FoxP3⁺ Treg differentiation. SOCS3 knockdown was used to evaluate rescue effects. H. pylori significantly promoted M1 macrophage polarization, with increased CD86, iNOS, MHC II, TNF-α, and IFN-γ and decreased CD163, Arg1, TGF-β, and IL-10 (p < 0.05). H. pylori also upregulated JAK3, STAT5, and SOCS3, while Ritlecitinib attenuated inflammatory gene expression (p < 0.05). Hp-CM significantly inhibited primary CD4⁺ T-cell proliferation, CD25/CD69 activation, and CD4⁺CD25⁺FoxP3⁺ Treg differentiation (p < 0.05). SOCS3 knockdown partially restored these CD4⁺ T-cell responses (p < 0.05). H. pylori promotes M1 macrophage polarization and impairs CD4⁺ T-cell immunity through JAK3/STAT5-SOCS3-mediated immune dysregulation. This mechanism contributes to chronic immune dysregulation and supports bacterial persistence, identifying JAK3/SOCS3 as potential therapeutic targets. - Source: PubMed
Publication date: 2026/08/11
Chen JianZhou LiLi LingWang Yue - Shenqi Compound (SQC) is effective in treating type 2 diabetes mellitus (T2DM). Preliminary clinical observations suggest that it may also improve pancreatic fibrosis in T2DM patients with comorbid chronic pancreatitis (CP), which prompted this mechanistic study. - Source: PubMed
Publication date: 2026/08/06
Su YiYang HengGong XianruZhang JiahongChen YunhuiLi XianglongPeng RuiZeji ZhimaLeng YulinFu Xiaoxu - Chronic kidney disease (CKD) is an independent risk factor for acute myocardial infarction (AMI), but the mechanisms underlying their comorbidity remain unclear. As a newly described inflammatory form of programmed cell death, PANoptosis may play a key role. This study aimed to identify shared pathogenic mechanisms and key targets linking the two diseases. - Source: PubMed
Publication date: 2026/07/22
Liu GuoyongXian HongliXu YehaoMa JunHuang JingyiYe Lili - Myocardial infarction (MI) is a critical cardiovascular event with a complex pathophysiology. This study aimed to investigate the role of the adipocytokine signaling pathway in MI, assess its potential association with diagnostic features, and explore its association with molecular subtypes. - Source: PubMed
Publication date: 2026/07/30
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