CCL26 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- CCL26 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00010344-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CCL26 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: CCL26 293T Cell Transient Overexpression Lysate(Denatured)
- 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: CCL26 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: CCL26 293T Cell Transient Overexpression Lysate(Denatured)
- Chemokine (C-C motif) ligand 26 (CCL26), also known as eotaxin-3, is an immune-regulatory chemokine involved in inflammatory responses and immune cell recruitment. Emerging evidence suggests its expression is dysregulated across multiple malignancies, yet comprehensive pan-cancer evaluations remain limited. - Source: PubMed
Ali SIsmail MKumar PMohamed SAlyoubi WMohamed HAlamri RYasin FAbdelrahman SAlshaibi HOsman EFozilovna ABadritdnova MAkasha RAlfaki M - Eosinophilic chronic rhinosinusitis (CRS), characterized by prominent eosinophil infiltration, has the highest postoperative recurrence rate among CRS subtypes. Given the critical role of eotaxins in CRS pathogenesis, this study aimed to identify eotaxins associated with eosinophilic CRS and evaluate their correlation with surgical outcomes. Transcriptomic data from GSE36830 revealed 125 differentially expressed genes (49 up-regulated, 76 down-regulated) in CRSwNP compared to CRSsNP, with significant enrichment of eosinophil and dendritic cell infiltration pathways. Functional analysis identified chemotaxis and cell migration as key dysregulated processes in CRSwNP. Among eotaxins, CCL26 and CCL13 emerged as hub molecules from the intersection of these dysregulated pathways. In a clinical cohort of 115 CRS patients, preoperative serum CCL26 and CCL13 levels were significantly elevated in CRSwNP compared to CRSsNP (P<0.001). ROC analysis demonstrated strong diagnostic power for nasal polyps (CCL26: AUC=0.895; CCL13: AUC=0.830). Higher preoperative CCL26 levels predicted poorer symptom improvement post-surgery (standardized β=-0.564, P<0.001). In conclusion, preoperative serum CCL26 serves as both a diagnostic biomarker for CRSwNP and a prognostic indicator for surgical outcomes, with elevated levels associated with reduced symptom improvement. - Source: PubMed
Publication date: 2026/08/07
Wang XudongLiu ShunanChen JichuanZeng WantingJiang Jianguo - Mugwort () is a predominant aeroallergen for allergic rhinitis (AR) in northern China. However, the molecular changes linking local nasal mucosal inflammation with systemic alterations remain incompletely understood. This study aimed to explore the cross-level regulatory network in a mouse model of mugwort-induced AR by combining nasal mucosal transcriptomics and serum metabolomics. - Source: PubMed
Publication date: 2026/07/08
Chi JiaoniChen LinJin YuxuanSun Jin-LyuXu Yajie - Severe asthma is a heterogeneous disease. The mechanisms driving airway pathology when type 2 (T2) cytokine activity is suppressed remain poorly understood. This study aimed to provide insight by identifying the airway molecular pathways of T2 biomarker-high and -low severe asthma. We analysed clinical and transcriptomic data from bronchial biopsies and brushes in the UK Refractory Asthma Stratification Programme multi-centre severe asthma cohort (18 corticosteroid-resistant T2 biomarker-high [T2-high], 23 T2 biomarker-intermediate [T2-intermediate], 11 T2 biomarker-low [T2-low]) plus 20 healthy controls pre- and post-treatment with high-dose inhaled corticosteroids (ICS). Many genes dysregulated in asthma vs. health were concordantly dysregulated in healthy subjects receiving ICS. Severe asthma as a whole, independent of confounding by ICS, was characterised by upregulation of mucins, CEACAM5, typical T2-genes (POSTN, CLCA1, CCL26), epithelial mast cell genes, and CPA4. T2-high severe asthma demonstrated upregulated T2-dependent genes, epithelial barrier and keratin genes, adaptive immune responses, and impaired ciliary function. T2-low asthma showed upregulated Th1- and IL-17-associated genes (IDO1, CXCL10, GBP1, LAG3), interferon-γ signalling, neuroimmune pathways, airway smooth muscle-related genes, and neutrophil enrichment. T2-intermediate asthma exhibited a mixed molecular profile sharing features of T2-high and T2-low endotypes, with selective expression of the pathogen defence and antiviral response genes. The results were validated using bronchoscopy data from the U-BIOPRED Consortium. This study defines airway molecular endotypes of severe asthma associated with T2 biomarker high and low phenotypes, independent of corticosteroid effects. These findings offer insights for severe asthma management and the development of targeted biologic therapies. - Source: PubMed
Publication date: 2026/07/20
Shen JiashuChaudhuri RekhaBicknell StephenMansur Adel HShrimanker RahulPavord Ian DFowler Stephen JBrown VanessaMcGarvey Lorcan PHowarth Peter HDahlén Sven-ErikAdcock Ian MZounemat-Kermani NazaninArron Joseph RHeaney Liam GChoy David FHinks Timothy S CMarchi EmanueleBradding Peter - The mechanisms responsible for promoting allergic asthma remain incompletely understood, particularly the role of the crosstalk between innate immune cells and airway epithelium in coordinating the response to inhaled allergen. - Source: PubMed
Publication date: 2026/07/15
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