Proteins CCL26 24-94_Eotaxin-3 , Human
- Known as:
- Proteins CCL26 24-94_Eotaxin-3 , Human
- Catalog number:
- C113
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins CCL26 24-94_Eotaxin-3 Human
Related genes to: Proteins CCL26 24-94_Eotaxin-3 , Human
- Gene:
- CCL26 NIH gene
- Name:
- C-C motif chemokine ligand 26
- Previous symbol:
- SCYA26
- Synonyms:
- MIP-4alpha, eotaxin-3, IMAC, MIP-4a, TSC-1
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-09
- Date modifiied:
- 2016-10-05
Related products to: Proteins CCL26 24-94_Eotaxin-3 , Human
Related articles to: Proteins CCL26 24-94_Eotaxin-3 , Human
- Chronic rhinosinusitis with nasal polyp (CRSwNP) is a heterogeneous Type 2 inflammatory disease characterized by enhanced eosinophilic infiltration. Both innate and adaptive immunity are involved in the onset and progression of CRSwNP. Increased serum leptin levels are associated with various allergic conditions; however, the biological role of leptin in allergic immune cells requires further investigation. - Source: PubMed
Publication date: 2026/04/17
Sonoda YukiSato YoheiImoto YoshimasaTamari MayumiFujieda Shigeharu - The molecular link between Hepatitis B virus (HBV) infection and hepatocellular carcinoma (HCC) progression remains elusive. Here, we identify glutathione peroxidase 2 (GPX2) as a pivotal mediator of this process. Single-cell analysis of HBV-positive HCC reveals a distinct GPX2 CSC population characterized by high MYC and CD44 expression. We demonstrate that GPX2 preserves stemness intrinsically by mitigating ROS-mediated c-MYC nuclear-cytoplasmic distribution, while extrinsically fostering immune evasion via the CCL26-CCR3 signaling axis. specifically, GPX2-derived CCL26 recruits and educates B cells towards an immunosuppressive LGALS1 state, which predicts adverse patient outcomes. , GPX2 overexpression accelerates tumorigenesis, whereas targeting CCR3 with ALK4290 sensitizes tumors to anti-PD-1 checkpoint blockade. These findings delineate a dual mechanism whereby GPX2 couples oxidative stress regulation to immune modulation, positioning the GPX2-B cell axis as a promising therapeutic target for HBV-driven liver cancer. - Source: PubMed
Publication date: 2026/03/20
Lin LiangYang ShiyeZhang JixiangChen GuoduZhou WuhanChen DongxingChen Jiafei - The airway epithelium serves as the initial barrier of defence in the respiratory system, guarding against microbial, chemical, and environmental threats introduced through inhaled air. Pattern recognition receptors within the airway epithelium facilitate the detection of these threats. Toll-like receptor-3 (TLR3), a receptor sensitive to double-stranded RNA viruses, plays a vital role in this sensing process. This study focuses on exploring the role of the Forkhead box protein O1 (FOXO1) in airway epithelial cells. While the FOXO1 transcription factor (TF) has been extensively examined in various cell types and diseases, its role in airway epithelial cells is not fully elucidated. FOXO1 expression was altered in the BEAS-2B airway epithelial cell line using a shRNA lentivirus for knockdown and a constitutively active FOXO1 plasmid (CA-FOXO1) for overexpression. Confirmation of FOXO1 knockdown/overexpression was achieved through qRT-PCR, immunofluorescence, and Western blotting. FOXO1 activity was impeded using the FOXO1 inhibitor AS1842856 in BEAS-2B and normal human bronchial epithelial (NHBE) cells. TLR3 expression was assessed through qRT-PCR and Western blot. Inflammatory cytokines/chemokines IL6, CXCL10, TSLP, CCL26, IL8, GM-CSF, IFN-λ1, TNF-α and CCL2 were analyzed using MSD Immunoassays after stimulation with TLR3 ligand Poly(I:C). ECIS analysis demonstrated that FOXO1-deficient airway epithelial cells exhibit enhanced recovery of barrier integrity following wounding, with faster restoration and higher resistance compared to control cells. FOXO1-deficient BEAS-2B cells exhibited reduced TLR3 mRNA expression while cells transfected with constitutively active FOXO1 displayed increased TLR3 mRNA expression, without corresponding changes in TLR3 protein levels. Inhibition of FOXO1 activity reduced TLR3 mRNA expression in BEAS-2B and NHBE cells. Co-treatment of BEAS-2B cells with the FOXO1 inhibitor and Poly(I:C), resulted in lower IL6 and CCL2 release compared to stimulation with Poly(I:C) alone, but did not affect the release of the other cytokines/chemokines measured. Finally, Poly(I:C) stimulation induced a time-dependent increase in FOXO1 nuclear localization in airway epithelial cells. FOXO1 depletion had no effect on RIG-I, MAVS, or MYD88 expression, suggesting selective regulation of TLR3 among antiviral RNA-sensing pathways. FOXO1 inhibition in SARS-CoV-2-infected NHBE cells significantly reduced viral spike RNA levels 24 h post-infection. Furthermore, we showed that FOXO1 knockdown did not affect cell proliferation, or cell death. In-silico analysis suggested that FOXO1 can bind to the TLR3 promoter, but our EMSA data were inconclusive. These findings indicate that FOXO1 selectively modulates airway epithelial inflammatory and barrier responses. FOXO1 inhibition may have therapeutic potential in mitigating airway inflammation. However, further studies are needed to elucidate the underlying mechanisms of FOXO1-mediated TLR3 regulation. - Source: PubMed
Publication date: 2026/04/03
Daniel Nadia MMann-Nüttel RituShrestha Palikhe NamiLópez-Orozco JoaquinHobman TomForsythe PaulVliagoftis Harissios - Tumor cells adapt to hypoxia by releasing hiTDExs enriched with bioactive molecules that modulate endothelial behavior and promote tumor progression. This study aimed to characterize how hypoxia-induced HNSCC exosomes reshape the endothelial secretome and contribute to metastatic potential. - Source: PubMed
Publication date: 2026/04/03
Capik OzelTekman SevilGundogdu BetulKilic AhsenPolat RumeysaAydin OmerKaratas Omer Faruk - Celastrol, a bioactive compound from Tripterygium wilfordii Hook F, has been reported to exert potent anti-inflammatory effects through multiple signaling pathways. While its activity has been studied in various cell types and disease models, its effects in atopic dermatitis (AD) is limited to a few studies in mouse models and remains largely unexplored in in vitro cell models. In this study, anti-inflammatory effects of celastrol were assessed in Th1-driven 2D inflammation models of HaCaT keratinocytes and dermal fibroblasts (DF), and in a Th2-driven 3D AD skin model. Cytokine stimulation mimicked chronic inflammation. Celastrol was applied at sub-cytotoxic concentrations, and inflammatory markers were quantified on the mRNA (qPCR) and protein (ELISA) level. In 2D models, celastrol reduced interleukin (IL)-8 and IL-6 secretion in a concentration-dependent manner, with fibroblasts producing higher cytokine levels than keratinocytes. In 3D AD models, topical celastrol (10 µM) was well tolerated and markedly reduced secretion of IL-8, IL-6, IL-1α, and mRNA expression of CXCL8, IL6, IL1B, and IL23A, even under continuous Th2 stimulation. AD biomarker genes CCL26, CA2, and NELL2 were unaffected, likely due to persistent cytokine exposure. Celastrol displayed strong anti-inflammatory activity in both Th1- and Th2-driven in vitro skin inflammation models, including a physiologically relevant 3D AD model. Its multitarget action support its potential as a topical treatment candidate for chronic inflammatory skin diseases. - Source: PubMed
Publication date: 2026/04/02
Reddersen KirstenMorgner BiankaWerz OliverLorkowski StefanFischer DagmarTittelbach JörgWiegand Cornelia