Eotaxin _ CCL11
- Known as:
- Eotaxin _ CCL11
- Catalog number:
- GTX10369
- Product Quantity:
- 25 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- Eotaxin _ CCL11
Ask about this productRelated 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
- Heat stress (HS) affects female reproductive efficiency by disrupting redox homeostasis and activating inflammatory responses in the corpus luteum (CL), a metabolically active tissue essential for pregnancy maintenance. This study reveals the protective effect of resveratrol against HS-induced luteal injury in pregnant mice through the regulation of oxidative stress and cytokine-chemokine-mediated inflammatory and immune responses. The pregnant mice were divided into three groups: control, HS, and resveratrol +HS. Heat stress was applied at 40 ± 0.5 °C for 7 days, with resveratrol (10 mg/kg) given orally 2 h before exposure to HS. The results showed that heat exposure reduced serum total superoxide dismutase activity and increased malondialdehyde level, causing significant disruption of luteal morphology with cellular disorder and vacuolization, which was partially overcome by resveratrol pretreatment. Transcriptomic profiling showed that HS induced a strong immunological and inflammatory response, involving cytokine-cytokine receptor interaction and chemokine signaling. Resveratrol significantly attenuated HS-induced transcriptional changes. The RT-qPCR results showed that HS increased chemokine ligands (, , ) and cytokine receptors , , ), which were suppressed by resveratrol. The chemokine-based inflammatory module is one of the most important regulatory properties of the HS response, according to the network analysis. Stable binding of resveratrol with major chemokine receptors was supported by molecular docking and molecular dynamics simulations. Collectively, HS induces oxidative, structural, and inflammatory alterations in luteal tissue, while resveratrol attenuates these changes by being associated with improved antioxidant status and suppression of cytokine-chemokine-mediated responses. - Source: PubMed
Publication date: 2026/04/14
Tariq MuhammadQuddus AbdulVictor Kossinga Koulet André SaintBeshah Kebede HabtegiorgisYan YexiaoMao Dagan - To identify candidate biomarkers of blood stasis syndrome (BSS) associated with coronary artery disease (CAD) and explore the underlying inflammatory mechanisms. - Source: PubMed
Hongzheng L IGuosheng LinYuxuan PengAlexey Viktorovich ChurovWenwen YangJie WangJieming L UFeifei LiaoRuotong Y UYue WeiZhiru ZhaoAimei L UPeng L IAling ShenLinzi LongHua Q UChanggeng F U - - Source: PubMed
Publication date: 2026/04/21
Yang Hyun-WooJo Yeong-InYang Hwa-EunPark Joo-HooSon Hyeong-GukMoon Jee WonPark Il-Ho - Recent studies have highlighted the critical role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3) in inflammation, with inhibitors like 3PO showing therapeutic potential in various inflammatory diseases. However, its effect on asthma inflammation remains unclear. - Source: PubMed
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Huang SiqingWei ShunaLuo FangCheng Yuanxiong - Chronic systemic inflammation and DNA methylation changes are two major hallmarks of aging, yet their interaction is poorly known. We investigated the relation between circulating inflammatory proteome and epigenetic age acceleration as assessed by DNA methylation in four independent cohorts of different ages and health conditions. Epigenetic age scores known to predict human health span (GrimAge and PhenoAge) were more strongly associated with age-associated inflammatory proteins, frailty, and multimorbidity when compared to epigenetic age scores associated with lifespan (Horvath and Hannum). Mendelian randomization analyses showed that blood concentrations of important inflammatory cytokines associated with the interferon pathway (CXCL9, CXCL10, CCL11, and IL-18) increase with age and are causal drivers of epigenetic age acceleration and age-related diseases. Furthermore, aging was associated with dysregulation of cytokine production capacity in immune cells in response to microbial stimulation. These findings argue that the interferon pathway may represent a target for anti-aging interventions. - Source: PubMed
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