ELISA Human , MCP-1 , Sensitive
- Known as:
- Enzyme-linked immunosorbent assay test Human , MCP-1 , Sensitive
- Catalog number:
- RBMS281R
- Product Quantity:
- 96 wells (1 kit)
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- ELISA Human MCP-1 Sensitive
Related genes to: ELISA Human , MCP-1 , Sensitive
- 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: ELISA Human , MCP-1 , Sensitive
Related articles to: ELISA Human , MCP-1 , Sensitive
- Conventional fractionated radiotherapy (CFRT) remains a mainstay for many solid tumors, yet it often fails to elicit durable anti-tumor immunity. How CFRT engages tumor-cell programs to shape the immune microenvironment and determine therapeutic outcome remains unclear. Here we show in preclinical mouse models that CFRT is associated with increased tumor-cell HMGB1 relative to stereotactic body radiotherapy (SBRT), and that loss of tumor-cell HMGB1 eliminates the efficacy gap between the regimens. HMGB1 deficiency markedly restrains tumor progression under CFRT in immunocompetent, but not immunodeficient, hosts, accompanied by increased intratumoral CD8 T cells and effector function. In esophageal squamous cell carcinoma (ESCC) specimens from patients receiving CFRT plus platinum-based chemotherapy, tumor-cell HMGB1 increases after treatment, and elevated pretreatment HMGB1 is associated with poor treatment response, reduced post-treatment CD8 T-cell infiltration, and adverse outcomes. Mechanistically, HMGB1 restrains CFRT-induced CD8 T-cell immunity through two convergent arms: CCL2-CCR2-dependent accumulation of suppressive monocytes and FUT8-linked regulation of PD-L1 fucosylation in tumor cells. TCF4 is linked to HMGB1-dependent induction of CCL2 and FUT8. Blocking CCL2 or inhibiting PD-L1 fucosylation restores CD8 T-cell effector function and enhances CFRT efficacy, alone or in combination with anti-PD-1 therapy. Together, these findings identify a tumor-cell HMGB1 program that underpins CFRT-associated immune suppression and nominate actionable targets to improve CFRT-immunotherapy combinations. - Source: PubMed
Publication date: 2026/09/19
Chen ChenShi JiahongCao PeihaiBai JuanLei YutiantianHuang MengdiSi MingjunWang RuiyingLv TingtingJia RuiMu QiuyuJiang DinggeHou YuzhuHuang Shan - Hyperammonemic rats show neuroinflammation and enhanced GABAergic neurotransmission in cerebellum. Treating hyperammonemic rats with compounds that reduce GABA receptors activation reduces some aspects of neuroinflammation. How GABAergic neurotransmission affects glial activation and the mechanisms involved are not clear. We hypothesized that, in cerebellum of hyperammonemic rats, enhanced GABA receptors activation contributes to activation of microglia, which releases pro-inflammatory factors that activate astrocytes, and that blocking GABA receptors with bicuculline will reverse these effects. The first aim was to characterize the effects of reducing GABA receptors activation with bicuculline in cerebellum of hyperammonemic rats on microglia and astrocytes activation. Neuroinflammation enhances GABAergic neurotransmission in cerebellum of hyperammonemic rats by activating the TNFα-TNFR1-S1PR2-CCl2-CCR2-BDNF-TrkB pathway and the TNFα-TNFR1-NFkB-glutaminase-GAT3 pathway. The second aim of this work was to assess if GABA receptors over-activation contributes to enhance activation of these pathways by analyzing if it is reversed by bicuculline. Hyperammonemia induces pro-inflammatory microglia activation, increasing NFκB, MAPK p38, STAT3, TNFα and glutaminase in microglia and TNFα, IL-1α and C1q which induce astrocytes activation. Enhanced GABA receptors activation also contributes to activate the TNFα-TNFR1-S1PR2-CCl2-CCR2-BDNF-TrkB, and TNFα-TNFR1-NFkB-glutaminase-GAT3 pathways. All these effects are reversed in cerebellar slices from hyperammonemic rats by blocking GABA receptors with bicuculline, indicating that are triggered by GABA receptors over-activation. These data support that enhanced GABA receptors activation in cerebellum induces pro-inflammatory effects in hyperammonemic rats and anti-inflammatory effects in control rats. - Source: PubMed
Publication date: 2026/09/19
Palomares-Rodriguez AndreaArenas Yaiza MFelipo Vicente - Peritoneal metastasis is the most devastating form of progression of gastric cancer, characterized by strong immune suppressive properties and resistance to treatment. Tumor-associated macrophages (TAMs) are the main population of immune cells in the peritoneal cavity and participate in nearly every step of this process. In this Review, we focus on the two major origins of peritoneal macrophages (embryonic-derived GATA6+ resident cells and monocyte-derived CCR2+ cells), and we describe how gastric cancer cells exploit their plasticity by metabolic signals, exosomal oncomiRs, paracrine factors and so on to push them into a pro-metastatic phenotype. Reprogrammed macrophages proceed to participate in detachment of tumor cells, resistance to anoikis, escaping across mesothelium and stimulating angiogenesis and lymphangiogenesis, but also instigate an immunosuppressive environment suppressing T cell activity and increasing chemoresistance. Important molecular players that we describe here are CCL2/CCR2 and CSF-1/CSF-1R signaling axes, the STAT3/STAT6/PI3K axis and a complement-driven switch of TAMs from a cathepsin (CTS)-high to complement component 1q(C1q)-high state that promotes immune evasion. We also discuss the role of exosome-mediated cross-talk and give an overview of novel therapies against macrophages such as blocking their recruitment, reprogramming their polarization or using chimeric antigen receptor macrophage (CAR-M) therapy, typically in combination with hyperthermic intraperitoneal chemotherapy (HIPEC) or immune checkpoint inhibitors. Bringing together the latest advances, we highlight key gaps in our understanding and suggest a direction for dismantling the macrophage-orchestrated metastatic niche with the ultimate goal of improving outcomes of this devastating disease. - Source: PubMed
Publication date: 2026/09/02
Chen MinLi YuyangWang HuinanLi XuyangShen QianYang Lei - Immune checkpoint blockade has transformed treatment in selected gastrointestinal (GI) cancers, yet primary resistance, incomplete responses and acquired resistance remain common. This heterogeneity is not explained by tumour-cell genomics alone; extracellular signalling programmes within the tumour microenvironment can determine immune recruitment, access and adaptation to therapy. The tumour secretome-including cytokines, chemokines, growth factors, complement components, matricellular proteins, soluble checkpoint molecules and extracellular-vesicle-associated cargo-regulates immune-cell recruitment, exclusion, suppression, tertiary lymphoid structure formation and exhaustion across anatomical and molecular contexts. Across gastric and esophageal cancers, colorectal cancer, pancreatic ductal adenocarcinoma, hepatocellular carcinoma and biliary tract cancers, recurrent suppressive circuits include TGF-β, VEGF, CXCL12-CXCR4, CXCL8/IL-8-CXCR1/2, CCL2-CCR2, CSF1-CSF1R, IL-6-family cytokines, SPP1/osteopontin, periostin, galectins, DKK1, MIF, complement and soluble or vesicular PD-L1. Conversely, CXCL9/10/11-CXCR3 signalling and CXCL13-associated tertiary lymphoid structures characterise immune-permissive states that can support checkpoint responsiveness. We organise these circuits into four overlapping functional modules-myeloid-enriched, fibroblast-driven exclusion, angiogenic-immunosuppressive and immune-permissive-and apply a four-level evidence hierarchy that separates clinical validation from mechanistic inference. Clinically useful secretome biomarkers will therefore need to integrate cellular source, spatial localisation, receptor context, temporal dynamics and linkage to actionable immune-state transitions. - Source: PubMed
Publication date: 2026/09/11
Li KexunQian ZilongMao JieHan YongtaoLeng Xuefeng - This study established an integrated framework combining multi-omics analysis, machine learning (ML), single-cell RNA sequencing (scRNA-seq), molecular docking, and in vitro validation to investigate potential mechanisms and therapeutic targets of obesity-associated asthenozoospermia (AZS). Based on transcriptomic data from the Gene Expression Omnibus (GEO), differential expression analysis and weighted gene co-expression network analysis (WGCNA) identified 37 candidate genes enriched in cytokine-cytokine receptor interactions, tumor necrosis factor (TNF) signaling, and chemokine-related inflammatory pathways. Protein-protein interaction (PPI) analysis indicated CTSS as a hub gene. Among 113 ML models using 12 algorithms, glmBoost + LDA performed best and prioritized CCL2, CCL4, EDEM3, PHF3, and SLC38A2 as core biomarkers; Shapley additive explanations (SHAP) assessed their predictive contributions. Gene set enrichment analysis (GSEA), immune infiltration, and scRNA-seq analyses identified adipose tissue macrophages as a major cellular source of Ccl2/CCL2. However, as the scRNA-seq data were derived from mouse adipose tissue rather than human testis, this finding primarily serves to generate the hypothesis that macrophage-derived CCL2/CCR2 signaling may, in theory, contribute to testicular microenvironment disruption and Sertoli cell injury through inflammatory amplification and intercellular communication, rather than providing direct in vivo evidence of such cross-tissue transmission. Molecular docking, cellular thermal shift assay (CETSA), and TM4 cell experiments showed that palmatine modulated the CCL2/CCR2 axis and suppressed MAPK/NF-κB signaling, alleviating inflammation, apoptosis, and blood-testis barrier (BTB) injury. Collectively, the CCL2/CCR2 axis is suggested to act as a pathological bridge in the context of obesity-associated adipose inflammation and male reproductive dysfunction, with palmatine showing potential as a candidate compound for further mechanistic and translational investigation. These findings provide a testable hypothesis for future in vivo studies to determine whether the CCL2/CCR2 axis plays a causal role in obesity-associated AZS. - Source: PubMed
Publication date: 2026/09/01
Wang PengruiTeng FeiTong SiyuLi HaixinWang DingkunBai Fangfang