CCL17 _ TARC _ SCYA17 Protein (Native)
- Known as:
- CCL17 _ TARC _ SCYA17 Protein (Native)
- Catalog number:
- 10233-HNAB
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- CCL17 _ TARC SCYA17 Protein (Native)
Related genes to: CCL17 _ TARC _ SCYA17 Protein (Native)
- Gene:
- CCL17 NIH gene
- Name:
- C-C motif chemokine ligand 17
- Previous symbol:
- SCYA17
- Synonyms:
- TARC, ABCD-2
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-26
- Date modifiied:
- 2016-10-05
Related products to: CCL17 _ TARC _ SCYA17 Protein (Native)
Related articles to: CCL17 _ TARC _ SCYA17 Protein (Native)
- Muscle fibrosis is a key pathological feature of Duchenne muscular dystrophy (DMD) and is closely associated with disease progression. Fibroadipogenic progenitors (FAPs) are major contributors to fibrosis, yet the precise mechanisms remain unclear. To investigate FAP dynamics and lineage specification, we generated dual-reporter mice (PRURD2) by crossing D2.B10-Dmdmdx/J (D2-mdx) mice with FAP and brown/beige adipose tissue (BAT) reporter lines. Corresponding control mice (PRURDBA) were established on the DBA/2J background. At 12 months, heart, diaphragm, and tibialis anterior (TA) muscles were collected for histological analysis. FAPs were isolated via FACS and subjected to single-cell RNA sequencing. PRURD2 mice exhibited increased fibrosis across all muscles compared to controls ( < 0.01) and a significant rise in PDGFRα-GFP + FAPs ( < 0.05). UMAP clustering identified 11 distinct FAP subpopulations, with the fibrosis-associated CD55 cluster enriched in PRURD2 mice. Pseudotime analysis showed lineage progression from progenitor clusters toward the fibrogenic CD55 cluster. CellChat analysis indicated increased interactions in PRURD2 mice involving fibrosis-related pathways like COLLAGEN, TGF-β, WNT, NOTCH, and ANGPTL. Additionally, fibrosis-related signaling pathways such as THY1, TWEAK, EPHA, EPHB, and SEMA6 showed increased interactions among FAP clusters in PRURD2 mice. Differential gene expression analysis revealed top upregulated genes including , , and . PRURD2 mice develop severe fibrosis in skeletal and cardiac muscle, driven by FAP-induced signaling pathways and genes. This model is valuable for understanding muscle fibrosis in DMD and developing anti-fibrotic therapies. - Source: PubMed
Publication date: 2026/04/24
Fusagawa HiroyoriLau JustinSharma SankalpLiu MengyaoSamimi YusefFranchet-Schaer GabrielFang AshleyFusagawa MinamiKim HubertFeeley Brian TLiu Xuhui - Mycosis fungoides (MF) is a disease that evolves slowly over years with few options for curative treatment. Improving health-related quality of life (HRQoL) is therefore an important treatment goal. This study aims to contribute to a better understanding of HRQoL, using a dermatology-adapted HRQoL questionnaire, Dermatology Life Quality Index (DLQI), in patients with MF. Baseline data from a cohort study (BIO-MUSE) of patients with MF wasere used to investigate which aspect of DLQI is the most affected and how DLQI relates to different clinical and physiological parameters. Data from a period of 12 months were used to study how DLQI changes over time. The symptom domain, for example itching, was the aspect of the DLQI that had the greatest impact on HRQoL. Thymus and activation-regulated chemokine (TARC)/ chemokine (C-C) ligand 17 (CCL17) were analysed in blood and were shown to have a positive correlation with DLQI (r=0.482, p=0.043). It was further shown that increased itching at baseline was a strong predictor of a worse DLQI score in the domain of symptoms (r=0.677, p=0.002). Future research in a larger cohort is needed to investigate the effect of itch in HRQoLhealth-related quality of life in patients with MF. - Source: PubMed
Publication date: 2026/04/22
Hub DariaDrott KristinaBelfrage EmmaSonesson Andreas - Chemokine (CC motif) ligand 17 (CCL17), an inflammatory chemokine, has been shown to mediate pain and inflammation in animal models of arthritis. However, the specific molecular mechanisms by which CCL17 mediates its inflammatory functions remain largely unknown. Matrix metalloproteinases (MMPs), particularly MMP9 and MMP13, are cartilage degrading enzymes that are known to contribute to joint pain and inflammation in arthritis. These MMPs, produced in significant quantities by macrophages, facilitate the breakdown of the extracellular matrix and are regulated by various signaling pathways, including extracellular signal-related kinase (ERK1/2) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). However, how CCL17 regulates downstream mediators in arthritis has not yet been elucidated. This study investigates the regulatory role of CCL17 on MMP expression in peripheral blood mononuclear cells (PBMCs) and plasma from rheumatoid arthritis (RA) patients, as well as in monocyte-derived macrophages (MDMs) from healthy donors. Analysis of RA patient samples revealed a positive correlation between CCL17 levels and MMP9/MMP13 expression. Furthermore, CCL17 treatment of MDMs resulted in an upregulation of MMP9 and MMP13 expression, correlating with increased activity of ERK1/2 and NF-κB. Markedly, pre-treatment with pharmacological inhibitors, U0126 (an ERK1/2 inhibitor) and NF-κB Activation Inhibitor IV (NF-κB inhibitor), in both MDMs and RA PBMCs, demonstrated that CCL17-driven MMP9 and MMP13 expression was critically dependent on ERK1/2 and NF-κB activation. Our findings provide new insights into possible mechanisms driving joint destruction in RA, highlighting potential benefits of targeting CCL17 and/or its downstream mediators as potential therapeutic strategies for treating inflammation. - Source: PubMed
Publication date: 2026/04/20
Balendran ThivyaHourani TetianaGaneshalingam SubothiniHatch KatherineFletcher SamuelHor CecilLee Kevin M CHamilton John ALim KeithAchuthan Adrian A - Childhood obesity is a major predictor of lifelong chronic disease, yet the biological mechanisms linking early-life exposures to adiposity remain incompletely understood. Inflammatory and metabolic proteins have been implicated in obesity-related pathways, but their clinical utility in children is limited by biological variability and the invasiveness of sample collection. DNA methylation (DNAm)-derived protein proxies, or EpiScores, offer a stable, non-invasive alternative tool for capturing systemic physiological processes and may provide novel insights into the early biological embedding of obesity risk. - Source: PubMed
Publication date: 2026/04/21
Richter Erika MPatel PriyadarshniBabu Jeganathan RGeetha Thangiah - Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disorder driven by a combination of epidermal barrier dysfunction, immune dysregulation, and psychological stress. Although neuro-endocrine-immune interactions are known to contribute to the pathogenesis of AD, the key endocrine mediators and their molecular mechanisms require elucidation. Prolactin (PRL), a stress-associated hormone with cytokine-like immunomodulatory properties, has not been fully characterized in the context of AD. - Source: PubMed
Publication date: 2026/04/18
Li YuanyuanLi ZichenChen JiajieSui YuanLiu LuZhou JianweiDu WenqiangZhao RuiYong LiangLiu Shengxiu