Eotaxin _ CCL11
- Known as:
- Eotaxin _ CCL11
- Catalog number:
- GTX74044
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- Eotaxin _ CCL11
Related genes to: Eotaxin _ CCL11
- Gene:
- CCL11 NIH gene
- Name:
- C-C motif chemokine ligand 11
- Previous symbol:
- SCYA11
- Synonyms:
- eotaxin, MGC22554
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-24
- Date modifiied:
- 2016-10-05
Related products to: Eotaxin _ CCL11
Related articles to: Eotaxin _ CCL11
- Chronic rhinosinusitis with nasal polyps (CRSwNP) is a multifactorial inflammatory disease characterized by heterogeneous phenotypes and endotypes, necessitating personalized therapeutic strategies. Precision medicine approaches integrating molecular biomarkers may improve treatment selection and disease stratification. In this prospective controlled study, we investigated the tissue-level immunohistochemical effects of oral corticosteroids (OCSs) and topical steroids on the expression of periostin, eotaxin, interleukin-4 (IL-4), transforming growth factor-β (TGF-β), and tumor necrosis factor-α (TNF-α) in nasal polyp tissue. Sixty-five patients eligible for endoscopic sinus surgery (ESS) were enrolled and divided into two groups: Group 1 (n = 42) received topical steroids combined with oral prednisone (40 mg/day for 7 days preoperatively), whereas Group 2 (n = 23) received topical steroids alone. Immunohistochemical analysis demonstrated a significant reduction in periostin and eotaxin expression in both epithelial and stromal compartments following OCS therapy, accompanied by increased TGF-β expression. No significant differences were observed in IL-4 or TNF-α expression. These findings indicate that short-term OCSs selectively modulate molecular pathways associated with eosinophilic inflammation and tissue remodeling in CRSwNP, supporting biomarker-driven precision medicine strategies. - Source: PubMed
Publication date: 2026/05/19
Radajewski KamilBurduk PawełWierzchowska MałgorzataAntosik PaulinaJóźwicki JakubBurduk JakubGrzanka Dariusz - Hepatocellular carcinoma (HCC) is an aggressive malignancy with poor prognosis and a lack of reliable biomarkers. In this study, we integrated weighted gene co-expression network analysis, machine-learning-based prognosticmodelling, single-cell RNA sequencing, spatial transcriptomics, and molecular docking to identify angiogenesis-related drivers in HCC. SCAF1 was identified as a hub gene and was significantly upregulated in HCC tissues compared with normal liver tissues. High SCAF1 expression was closely associated with advanced clinicopathological features and unfavourable survival outcomes. The prognostic model constructed by machine learning showed robust predictive performance in both training and validation cohorts, and decision curve analysis supported its clinical utility. Single-cell and spatial transcriptomic analyses further suggested that SCAF1 was mainly associated with endothelial and immune-related features of the tumour microenvironment. Functional assays showed that SCAF1 knockdown suppressed HCC cell migration, invasion, VEGFA expression, and angiogenic capacity in vitro. Mechanistically, SCAF1 was negatively correlated with anti-angiogenic chemokines, including CCL19, CCL14, and CCL11, indicating a role in shaping a pro-angiogenic microenvironment. In addition, molecular docking identified genistein as a promising compound with stable binding to SCAF1. Experimental validation showed that genistein reduced SCAF1 and VEGFA expression and inhibited HCC cell proliferation, migration, invasion, and tube formation. Collectively, these findings suggest that SCAF1 is a novel prognostic and angiogenesis-related biomarker in HCC and a potential therapeutic target for genistein-based intervention. - Source: PubMed
Zheng HaoTang ShengweiShi RuidaYu ZichuanZhang RuiyuQu XiaoyuWan HaoFang ChenshuoWang XinZhu YeHuang DaChen Gen - Endoplasmic reticulum (ER) stress has emerged as a key player in the development of diverse chronic pain disorders; however, its specific contribution to migraine pathophysiology has yet to be fully elucidated. Although accumulating evidence indicates that transcutaneous auricular vagus nerve stimulation (taVNS) mitigates chronic pain, the precise molecular mechanisms governing this effect remain poorly understood. This study investigates the functional contribution of ER stress and its downstream signaling mechanisms in a nitroglycerin (NTG)-induced mouse model of chronic migraine, and whether taVNS exerts analgesic effects by modulating ER stress within trigeminal ganglion (TG) neurons. - Source: PubMed
Publication date: 2026/05/22
Lu Huan-JunHuang Meng-XuanWang Yi-FanRen Ning-YiDong Chun-YuLiu Meng-LuHuang Xin-YiGao Yong-JingWu Hao - Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder characterized by the deposition of amyloid-β (Aβ) in the walls of leptomeningeal and cortical blood vessels that increases risk of intracerebral hemorrhages and progressive cognitive decline. More than 90% of individuals with Alzheimer's disease (AD) exhibit some level of CAA. Notably, in the new era of disease-modifying treatments for AD, CAA is a significant risk factor for amyloid-related imaging abnormalities (ARIA), an adverse event associated with anti-amyloid treatments. Therefore, there is great need for accessible, reliable and accurate in vivo biomarkers (e.g., blood-based) to improve antemortem identification of CAA that would improve risk stratification and reduce symptomatic ARIA. In this study, we employed the Nucleic Acid-Linked Immuno-Sandwich Assay (NULISA™) central nervous system panel for exploratory biomarker quantification in antemortem plasma of participants with neuropathological assessments for CAA from the Banner Sun Health Research Institute Brain and Body Donation Program (N = 251) and independently validated in the University of California Irvine Alzheimer Disease Research Center cohort (N = 110). We evaluated the differential protein expression in antemortem plasma sample taken < 5 years (mean 1.76 ± 1.3) from death using a logistic regression model. We further compared multi-biomarker models and found that a combination of CRP, IL4, CCL11, NPY and PDLIM5, plus demographic covariates showed an area under the curve (AUC) of 0.90 (95% CI 0.86-0.94) to identify neuropathologically confirmed CAA in the discovery cohort. In our independent replication, the antemortem plasma signature performed better than the basic demographics model showing a potential to predict CAA. The exploration and validation in antemortem plasma indicate that a multi-analyte panel, when combined with in vivo blood biomarkers for AD pathology, may be capable of identifying the presence of CAA and could have an meaningful impact on the clinical evaluation of patients under the investigation for cognitive decline. Further developments in biomarkers for this condition are crucial so that CAA identification could inform treatment decisions by highlighting ARIA risk. - Source: PubMed
Publication date: 2026/05/20
Singh AlpanaDenkinger Marisa NLeuzy AntoineDieckhoff KariLiu JameMarques Taina MMonuki EdwinStark CraigGrill Joshua DHom ChristySultzer DavidDoran EricLott IraWood KevinGawronski BriannaGonzalez LourdesChoudhury ParichitaAtri AlirezaBeach Thomas GSerrano Geidy ESajjadi S AhmadVan Keuren-Jensen KendallReiman Eric MHead ElizabethAshton Nicholas J - Allergic rhinitis (AR) and asthma (AS) are closely linked in both epidemiology and pathogenesis, though the mechanisms remain unclear. This study aims to identify shared gene signatures and molecular mechanisms in the combined allergic rhinitis and asthma syndrome (CARAS) and validate these findings in a murine model. - Source: PubMed
Publication date: 2026/05/15
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