Cymax Human MCP-1 ELISA Kit
- Known as:
- Cymax Human MCP-1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- lf-ek0265
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Cymax Human MCP-1 ELISA Kit
Ask about this productRelated genes to: Cymax Human MCP-1 ELISA Kit
- Gene:
- CCL2 NIH gene
- Name:
- C-C motif chemokine ligand 2
- Previous symbol:
- SCYA2
- Synonyms:
- MCP1, MCP-1, MCAF, SMC-CF, GDCF-2, HC11, MGC9434
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-05
- Date modifiied:
- 2016-10-05
- Gene:
- SLC25A14 NIH gene
- Name:
- solute carrier family 25 member 14
- Previous symbol:
- -
- Synonyms:
- BMCP1, UCP5
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-09
- Date modifiied:
- 2016-10-05
Related products to: Cymax Human MCP-1 ELISA Kit
Related articles to: Cymax Human MCP-1 ELISA Kit
- Although Danzhi Jiangtang Capsule (DJC) is a traditional Chinese herbal preparation used clinically for diabetes, how it may protect the kidney during diabetic nephropathy (DN) has not been fully clarified. This investigation was designed to explore potential mechanisms by which DJC affects DN, with a focus on the NLR family pyrin domain-containing 3 (NLRP3)/Caspase-1/Gasdermin D (GSDMD) pyroptosis-related signaling cascade. An integrated strategy combining network pharmacology and machine learning was employed. The Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and the Bioinformatics Analysis Tool for Molecular Mechanism of Traditional Chinese Medicine (BATMAN-TCM) were used to screen bioactive ingredients and their corresponding protein targets of DJC. DN-associated genes were retrieved from Gene Expression Omnibus (GEO), GeneCards, and Online Mendelian Inheritance in Man (OMIM). Key candidate targets were screened and ranked using multiple machine learning algorithms. The binding affinity between DJC's active ingredients and core targets was assessed via molecular docking. Finally, the therapeutic efficacy and predicted mechanisms were evaluated in db/db diabetic mice. Network pharmacology analysis identified 599 DJC targets and 68 overlapping genes shared with DN. Using machine learning algorithms, C-C motif chemokine ligand 2 (CCL2) and CASP1 were identified as prioritized candidate targets. Molecular docking predicted possible strong binding affinities between DJC active ingredients and these core proteins. Functional enrichment analyses (GO/KEGG) suggested that DJC modulation is associated with inflammatory responses and the MAPK pathway. In vivo validation showed that DJC treatment attenuated renal injury and fibrosis markers. These findings suggest that DJC may attenuate DN in part through CCL2/C-C motif chemokine receptor 2 (CCR2)-related pyroptosis signaling changes. - Source: PubMed
Publication date: 2026/07/28
Li ZiqiangYuan YingZhao YueyueDeng YifangYin GangShen Anlu - Interferon (IFN) is an important treatment for chronic hepatitis B (CHB), with highly variable clinical efficacy, and how IFN-α mediates its therapeutic benefits via innate immunity, particularly macrophages, is not fully understood. - Source: PubMed
Publication date: 2026/08/05
Cai HaiyiZhou PeiZhu LifenLi RuiWang Yaping - To investigate longitudinal cellular and molecular immune remodeling during the transition from acute injury to chronic immunopathology after severe corneal alkali burn. - Source: PubMed
Lee YunjinYun Young InLee Soo JinKoh AhraSong HyunyoungLee Seung HyeunOh Ja YoungKim Kyoung Woo - CCR2+ monocytes are recruited to sites of acute myocardial injury, where they play a critical role in clearing necrotic debris and replenishing the depleted resident macrophage population. Although this response is necessary for early tissue repair, prolonged activation of inflammatory pathways and persistent recruitment of CCR2+ monocytes have been associated with accelerated ventricular remodeling and adverse outcomes. Inhibition of CCR2 has shown promise in preclinical models of myocardial injury and represents a potential therapeutic target. Cardiosphere-derived cell extracellular vesicles (CDC-EVs) have demonstrated cardioprotective effects partly through modulation of the immune response. We investigated whether CDC-EVs regulate inflammatory monocyte trafficking through effects on CCR2 signaling. We found that CDC-EVs reduce the surface availability of CCR2 on human monocytes through an miR-146a-dependent mechanism, resulting in decreased monocyte migration toward CCL2. These findings identify a previously unrecognized mechanism by which CDC-EVs modulate CCR2-dependent monocyte trafficking and provide new insight into how EVs regulate innate immune responses after myocardial injury. - Source: PubMed
Mentkowski Kyle ITarvirdizadeh ToubaPandey RohanSchiffmacher Paul JHough SaraEagler Lisa ASim Fraser JReynolds JessicaLang Jennifer K - Brain metastases (BrM) are a frequent and life-threatening complication of solid tumours, with lung cancer representing their most common source. While cancer-associated fibroblasts (CAFs) are well-established contributors to tumour progression in many extracranial malignancies, their presence and function within the brain tumour microenvironment, where fibroblasts have long been considered scarce or absent, remain poorly understood. Here, we isolated and characterised fibroblast-like cells from 13 human BrMs of diverse origins. These BrM-associated CAFs (BrM-CAFs) expressed canonical CAF markers and showed reduced proliferation and increased senescence compared to normal fibroblasts. Their transcriptome was enriched for extracellular matrix (ECM)-related genes, including multiple collagens, fibronectin, and matrix-remodelling enzymes. In vitro, BrM-CAFs produced a fibrillar ECM, and in BrM tissues, their abundance was associated with collagen I and fibronectin deposition. Transcriptomic, proteomic, and secretome analyses further revealed that BrM-CAFs produce multiple cytokines, chemokines, and growth factors that promote cell motility. BrM-CAF conditioned medium promoted both monocyte migration and the migration of cancer cells, including established cell lines and patient-derived lung cancer BrM cells; monocyte migration was partially reduced by inhibition of CCL2/CCR2 signalling, whereas blocking CXCL12, CXCL16, or CX3CL1 attenuated BrM-CAF-induced cancer cell migration. Beyond these effects on migration, exposure to BrM-CAFs increased cancer cell invasion in transwell and heterotypic 3D spheroid assays. In contrast, their effects on cancer cell proliferation were limited and did not indicate a growth-promoting role. Exposure to BrM-CAFs was also associated with increased expression of interferon-stimulated genes in cancer cells. Together, our findings support a role for BrM-CAFs in shaping the brain metastatic microenvironment through ECM remodelling and the secretion of pro-migratory mediators, promoting monocyte and cancer cell migration and enhancing cancer cell invasion. These data identify BrM-CAFs as active stromal participants in BrM biology and support further investigation of their biological, diagnostic, and therapeutic relevance. - Source: PubMed
Publication date: 2026/08/04
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