CCL11 Pre-design Chimera RNAi
- Known as:
- CCL11 Pre-design Chimera RNAi
- Catalog number:
- H00006356-R01
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CCL11 Pre-design Chimera RNAi
Related genes to: CCL11 Pre-design Chimera RNAi
- 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: CCL11 Pre-design Chimera RNAi
Related articles to: CCL11 Pre-design Chimera RNAi
- Aging entails complex physiological changes, yet large-scale evidence among older Japanese individuals, especially those with comorbidities, remains limited. We analyzed serum and plasma samples from approximately 3800 Japanese aged 40 years and older to identify age-associated proteins and lipids, focusing on reproducibility and robustness. Chemokines CXCL9 and CCL11 and phosphatidylcholines PC 31:0 and PC 32:0 were positively associated with age across five cohorts, whereas lysophosphatidylcholines LPC-LA and LPC-AA showed negative associations. These molecular relationships were consistently reproduced across serum and plasma matrices and replicated in independent cohorts. Cross-platform consistency was confirmed between Olink Target 96 (relative NPX) and Target 48 (absolute quantification), with direct validation in Cohort 2. To our knowledge, this is the largest study to demonstrate reproducibility of age-associated molecular biomarkers in a comorbidity-enriched Japanese population. The principal contribution is technical─defining a set of robust, cross-platform, cross-matrix biomarkers of aging in older adults. Unlike previous Western studies which focused on younger or healthier populations, this work establishes reproducibility and generalizability in real-world aging. These validated biomarkers provide a valuable reference for clinical and translational research, including risk stratification and biological age assessment in comorbidity-enriched settings. - Source: PubMed
Publication date: 2026/07/03
Tokuoka Suzumi MHamano FumieKobayashi AyakoNatsume TohruSugiyama MasayaMatsuda KoichiOda Yoshiya - Major depressive disorder (MDD) is a leading cause of disability worldwide. It remains elusive whether serum levels of cortisol, amino acids and their downstream neurotransmitters, and inflammatory cytokines can reflect the therapeutic response of MDD. Although music seems to be beneficial to MDD treatment, the optimal treatment strategy remains to be explored. Here, we report that the combination of pharmacotherapy and music therapy with both D major K. 448 and G minor K. 550, but not pharmacotherapy alone, significantly downregulated or presented numerical trends to downregulate serum levels of cortisol and norepinephrine (NE) in MDD patients. Furthermore, serum levels of L_Histidine, L_Glutamic acid, L_Aspartic acid, tumor necrosis factor-α (TNF-α), TNF-receptor I (TNFR I), and C-C motif ligand 11 (CCL11) were significantly downregulated or exhibited numerical trends to be downregulated by the combination of pharmacotherapy and music therapy, whereas those of cluster of differentiation 30 (CD30) exhibited opposite effects. Therefore, music therapy with both D major K. 448 and G minor K. 550 should be recommended as adjuvant therapy to MDD patients. Certain serum markers can reflect the therapeutic response of MDD. The therapeutic effects of music therapy may be attributed to augmented stress-coping ability and diminished systemic inflammation. - Source: PubMed
Publication date: 2026/06/30
Lu YuchenYao JunyuanGu Ke-ShengWu AnbiaoYang XiqinWu HaoXiao LijunZhang Jiyan - Plasticizers, including phthalate esters and phthalate-free alternatives, are widely detected environmental chemicals. Although increasing evidence suggests that plasticizers may disrupt gastrointestinal homeostasis, their potential molecular links with inflammatory gastrointestinal disorders (IGDs) remain unclear. - Source: PubMed
Publication date: 2026/06/07
Chen YongqiShi JiyuanRuan YunGuan JinghanYan MiaohanZhang ZongyingWu LuojinSang MengmengWang XinfengMao LimingLiu Zhaoxiu - Pulmonary arterial hypertension (PAH) is a fatal vascular disorder with poor prognosis. 6:2 chloro-polyfluorooctane ether sulfonate (F-53B), a persistent environmental contaminant detected in humans, is known to be vasculotoxic, yet its association with PAH remains unexplored. This study aims to elucidate the mechanisms linking F-53B exposure to PAH by integrating network toxicology, molecular docking and in vitro experiments. Potential F-53B targets were predicted using ChEMBL, PharmMapper, and TargetNet. PAH-related genes were compiled from GeneCards, Online Mendelian Inheritance in Man (OMIM), Therapeutic Target Database (TTD), and GSE254617. We identified 42 key targets of F-53B-related PAH. Functional enrichment revealed terms such as inflammatory response and extracellular matrix. Protein-protein interaction (PPI) analysis identified five hub genes: CCL2, CXCL8, CCL5, CCR2, and CCL11. Molecular docking confirmed strong binding between F-53B and these core targets, with CCR2 showing the strongest affinity (-10 kcal/mol). Molecular dynamics simulations further verified stable binding to CCR2. In vitro experiments demonstrated that F-53B activated the CCL2/CCR2 axis and induced IL-1β, TNF-α, and IL-6 in HUVECs and RAW264.7 cells. This study reveals that F-53B is linked to PAH through dysregulation of chemokine signaling networks and induction of inflammatory cytokines. These findings suggest F-53B as a potential environmental risk factor for PAH and pinpoint potential targets for intervention. - Source: PubMed
Publication date: 2026/05/29
Xu LinglingMa YujieZheng ZhenmingZou FeiLi Wenjun - Syphilis serofast, characterized by persistent seropositivity despite adequate treatment and symptom resolution, poses significant clinical challenges. This study investigated the immunological basis of serofast status, focusing on CD3 T-cell populations and cytokine profiles. - Source: PubMed
Publication date: 2026/06/20
Qiang DiPeng MinZhang WangyuTan Mengjun