STAT6 Antibody (Ab_645), pAb, Rabbit
- Known as:
- STAT6 Antibody (Ab_645), pAb, Rabbit
- Catalog number:
- A00284
- Product Quantity:
- 40ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- STAT6 Antibody (Ab_645) pAb Rabbit
Related genes to: STAT6 Antibody (Ab_645), pAb, Rabbit
- Gene:
- STAT6 NIH gene
- Name:
- signal transducer and activator of transcription 6
- Previous symbol:
- -
- Synonyms:
- D12S1644, IL-4-STAT
- Chromosome:
- 12q13
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-09
- Date modifiied:
- 2019-04-23
Related products to: STAT6 Antibody (Ab_645), pAb, Rabbit
Related articles to: STAT6 Antibody (Ab_645), pAb, Rabbit
- Chronic psychological stress promotes cancer progression by activating tumor-associated macrophages (TAMs), particularly through polarization toward the pro-tumorigenic M2 phenotype. However, therapeutic strategies targeting stress-induced macrophage polarization remain limited. This study investigated whether the ethanolic extract of Bupleurum falcatum L. root (EBF) can modulate chronic stress-driven TAM polarization. To simulate a stress-associated microenvironment, norepinephrine (NE) was used to treat 4 T1 breast cancer cells. Conditioned media from NE-treated cells (NE CM) significantly upregulated M2 macrophage markers and STAT6 phosphorylation in RAW 264.7 cells; however, these effects were markedly attenuated by EBF. Consequently, EBF inhibited M2 macrophage-induced cancer cell migration. Notably, EBF treatment modulated the tumor cell secretome, as CM from 4 T1 cells co-treated with NE and EBF failed to induce M2 polarization. Network pharmacology analysis identified interleukin (IL)-4 as a key mediator-upregulated by NE and suppressed by EBF-among the overlapping genes shared by cancer metastasis, BF, and M2 macrophage-associated gene sets. Furthermore, saikosaponins A, C, and D consistently contributed to these regulatory effects. Collectively, our findings demonstrate that EBF inhibits NE-driven M2 polarization and subsequent macrophage-mediated cancer progression, suggesting its potential as a therapeutic agent to modulate the tumor microenvironment under chronic stress conditions. - Source: PubMed
Publication date: 2026/07/06
Jeong Jae-HoonPark Shin-Hyung - Eosinophilic esophagitis (EoE) and atopy are associated with several genetic variants; however, their relationship with clinical features has been scarcely investigated. - Source: PubMed
Publication date: 2026/06/04
Rodríguez-Alcolado LeticiaNavares-Gómez MarcosCasabona-Francés SergioMolina-Infante JavierGuagnozzi DanilaSoria-Chacartegui PaulaFeo-Ortega SaraArias-González LauraTorres-Larrubia MacarenaLlerena-Castro RonaldMartín-Domínguez VerónicaZamorano JoseMolina-Jiménez FranciscaMajano Pedro LFernández-Pacheco JenniferRivas DoloresGrueso-Navarro ElenaZubiaur PabloSaiz-Rodríguez MiriamJuárez-Tosina RocíoAbad-Santos FranciscoSantander CecilioArias ÁngelLucendo Alfredo JLaserna-Mendieta Emilio J - Immune rejection after liver transplantation remains a major challenge impacting the long-term survival of liver transplant recipients. Inhibiting macrophage M1 polarization exerts a positive effect on alleviating post-transplant immune rejection. Arctiin, an active component derived from traditional Chinese medicine, may suppress macrophage M1 polarization by inhibiting the release of pro-inflammatory cytokines. This study employed experimental techniques including ELISA, double-label flow cytometry, Western blot analysis, and cellular immunofluorescence to investigate the potential mechanism underlying the effect of arctiin on macrophage M1/M2 phenotypic switching in vitro. Results demonstrated that arctiin promoted the conversion of M0 macrophages to the M2 phenotype, significantly downregulated the levels of pro-inflammatory cytokines IL-6 and TNF-α, inhibited the expression of the M1 macrophage marker inducible nitric oxide synthase (iNOS), and reduced the proportion of M1-type macrophages. Furthermore, arctiin notably enhanced STAT6 phosphorylation and TRAF6 protein expression in M1 macrophages while suppressing STAT1 phosphorylation. However, these beneficial effects of arctiin were significantly reversed by a CB2R antagonist. Additional experiments showed that a CB2R agonist exerted similar effects to arctiin. Treatment with a TRAF6 inhibitor abrogated the inhibitory effect of arctiin or the CB2R agonist on macrophage M1 polarization, increased STAT1 phosphorylation, and decreased STAT6 phosphorylation. In conclusion, this study indicates that arctiin can activate CB2R and exert anti-inflammatory effects through the TRAF6-STAT1/6 pathway, thereby promoting the phenotypic switch of macrophages from M1 to M2. - Source: PubMed
Publication date: 2026/07/04
Lin JieWang ChengyuHan LeiYuan Bo - Pulmonary fibrosis (PF) remains a lethal progressive disease with poorly defined molecular drivers. Epithelial dysfunction and metabolic reprogramming contribute to PF, but the mechanistic link between these processes remains unclear. Here, we identify a Kat5-STAT6 epigenetic-metabolic axis that governs fibrotic progression. Kat5 directly acetylates STAT6 at lysine 636 (K636), thereby suppressing STAT6 dimerization, phosphorylation and nuclear translocation. In fibrotic lungs, STAT6 acetylation at K636 is reduced, leading to its hyperactivation. Activated STAT6 drives transcription of pro-glycolytic enzyme hexokinase 2 (HK2), promoting metabolic reprogramming in alveolar type II (ATII) cells and extracellular matrix deposition. ATII cell-specific restoration of Kat5 rescues STAT6 acetylation, normalizes its activity and ameliorates fibrosis in vivo. Mechanistically, Kat5-mediated STAT6 acetylation functions as a biochemical brake that limits cooperation with profibrotic mediators such as tissue plasminogen activator (tPA). These findings redefine STAT6 regulation, highlight an acetylation-phosphorylation checkpoint controlling fibrogenesis, and suggest that Kat5 enhancers or STAT6 acetylation mimetics may represent potential therapeutic strategies for chronic lung disease. - Source: PubMed
Publication date: 2026/07/03
Yang YoujingLing YiLi JianzhongLi QianminFeng YanmeiXiao JunMa YuTao Shasha - Macrophages are key immune defenders in hydatid disease. While M1 macrophages express iNOS and M2 macrophages express TGF-β, the relationship between STAT6 activation and macrophage subsets remains unclear in hydatid disease. - Source: PubMed
Publication date: 2026/07/02
Elhamed Sara Mohamed AbdSweed DinaSallam HebatallahSabry Shaymaa