Mouse CCL11 ELISA Kit
- Known as:
- Mouse CCL11 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- orb55138
- Product Quantity:
- 10 plates
- Category:
- Peptides
- Supplier:
- Biorb
- Gene target:
- Mouse CCL11 ELISA Kit
Related genes to: Mouse CCL11 ELISA Kit
- 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: Mouse CCL11 ELISA Kit
Related articles to: Mouse CCL11 ELISA Kit
- 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
Publication date: 2026/05/14
Zhao XinlanHe ZhujingCao XiaoliLiu JiahuiDai ChunWang Mei - Eosinophils, traditionally viewed as effector cells in allergic and parasitic responses, have emerged as multifaceted regulators within the tumor microenvironment (TME). In lung cancer, eosinophils demonstrate complex and context-dependent functions, shaped by chemokines, cytokines, and tumor-derived signals such as CCL11 and IL-33. Recent studies indicate that eosinophils may either promote anti-tumor immunity, by enhancing CD8 T cell infiltration, secreting cytotoxic granules, and cooperating with IL-33, or facilitate tumor progression through recruitment of regulatory T cells, immune suppression, and expression of immunoregulatory enzymes like IDO. Moreover, eosinophil abundance in tumor tissues and peripheral blood has been associated with both favorable and unfavorable prognostic outcomes in lung cancer patients. Notably, elevated eosinophil counts correlate with improved responses to immune checkpoint inhibitors (ICIs), positioning them as potential biomarkers for immunotherapy efficacy. However, distinctions between tumor-infiltrating and circulating eosinophils, as well as their dualistic roles in metastasis and immune modulation, remain incompletely understood. This review summarizes current advances in understanding eosinophil biology in lung cancer and underscores their promise as diagnostic and therapeutic targets in precision immuno-oncology. - Source: PubMed
Publication date: 2026/04/28
Wang ZhenJiao FuzhiYuan JingZhang ShengnanShi Fenglei - : Recurrence poses a major challenge in epithelial ovarian cancer (EOC), often occurring despite optimal first-line therapy. Dormant cancer cells are believed to play a key role, yet the mechanisms driving their reactivation remain unclear. This study examined whether exosomes released by normal peritoneal mesothelial cells (PMCs) and fibroblasts (PFBs) undergoing iatrogenic senescence after carboplatin and paclitaxel exposure contribute to EOC recurrence. : Senescent PMCs and PFBs secreted markedly more exosomes, identified by CD9, CD63, and CD81, compared with young cells. Exosomes from both cell types more effectively reactivated dormant EOC cells (pEOCs, A2780, OVCAR-3, SKOV-3) than non-exosomal medium constituents. Importantly, senescent PMC-derived exosomes most strongly reactivated pEOCs and SKOV-3, whereas those from senescent PFBs exerted greater effects on pEOCs, OVCAR-3, and SKOV-3. Kinetic studies of exosome internalization revealed that this process was generally more efficient in the presence of exosomes derived from senescent cells compared with those from young donor cells. Compositional analysis revealed distinct profiles between young and senescent exosomes compared in two variants: young PMCs/senescent PMCs and young PFBs/senescent PFBS. Senescent PMC exosomes displayed reduced miR-210-3p, miR-409-3p, and miR-421, alongside elevated MMP1, MMP3, and VEGF, while senescent PFB exosomes showed increased amphiregulin and osteopontin but lower MMP1, MMP3, TIMP1, bFGF, VEGF, and HGF. Functionally, senescent PMC exosomes enhanced pEOC migration, invasion, and spheroid formation, and induced the expression of CCL11 and ABCB1. Senescent PFB exosomes promoted migration and upregulated CCL11, TGF-β1, BIRC5, and CHEK1. : These findings suggest that therapy-induced senescence in peritoneal cells may contribute to EOC recurrence by reactivating dormant tumor cells through exosomal signaling. - Source: PubMed
Publication date: 2026/04/23
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