Recombinant Human Eotaxin _ CCL11
- Known as:
- Recombinant Human Eotaxin _ CCL11
- Catalog number:
- 228-10396-2
- Product Quantity:
- 20
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Recombinant Human Eotaxin _ CCL11
Related genes to: Recombinant Human 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: Recombinant Human Eotaxin _ CCL11
Related articles to: Recombinant Human Eotaxin _ CCL11
- 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
Wang ZhuiyueChen JingZhang YuanyuanZhao XiaomanShen ShipingZhang XinguangYao WenboLiu YazunXue Zheng - Lymph node metastasis (LNM) is a primary critical factor for gastric cancer (GC) prognosis, fundamentally driven by the adaptive remodeling of the tumor microenvironment (TME). While gastric cancer-associated mesenchymal stem cells (GCMSCs) are recognized as pivotal orchestrators of the tumor niche, the paracrine mediators governing LNM remain poorly defined. In this study, integrative transcriptomic and cytokine profiling identified CCL11 as the most significantly upregulated chemokine in GCMSCs. Clinical analysis demonstrated that elevated CCL11 expression in tumor tissues correlated with advanced LNM and dismal overall survival. Furthermore, a signature score derived from CCL11 MSC subclusters, identified via single-cell RNA sequencing, was positively associated with advanced clinical stages and poor prognosis. Serum CCL11 levels further exhibited high diagnostic efficacy for gastric cancer (AUC:0.8131) and moderate predictive value for lymph node metastasis (AUC:0.7848). Intriguingly, despite these robust clinical associations, exogenous CCL11 failed to directly influence the proliferative or migratory capacity of GC cell lines. This discrepancy was resolved by our finding that the cognate receptor CCR3 was virtually absent on the malignant epithelium but selectively enriched on macrophages and lymphatic endothelial cells (LECs). Functionally, GCMSC-derived CCL11 drove M2 macrophage polarization to bolster tumor stemness and chemoresistance, while simultaneously remodeling LECs to facilitate lymphangiogenesis and transendothelial migration. Mechanistically, hypoxic stress triggered the nuclear translocation of TCF21, which directly transactivated the CCL11 promoter in GCMSCs. Together, these findings identify the hypoxia-TCF21-CCL11 axis as a key driver of the GC metastatic niche, highlighting the indispensable significance of stromal-derived molecules in deciphering metastatic complexity and identifying promising targets for early diagnosis and strategic therapeutic intervention. - Source: PubMed
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