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
- Cytokines and chemokines are central mediators of inflammation and immune dysregulation in diabetes mellitus, linking metabolic stress to tissue injury across diverse disease types and complications. In type 1 diabetes (T1D), pro-inflammatory cytokines such as IL-1β, TNF-α, and IFN-γ drive autoimmune β-cell destruction, amplified by chemokines like CXCL10 that recruit autoreactive T cells. In type 2 diabetes (T2D), obesity-associated metaflammation is characterized by chronic low-grade elevations in IL-6, IL-1β, TNF-α, and chemokines, including CCL2, which promote insulin resistance and β-cell stress. Gestational diabetes (GDM) reflects heightened placental cytokine and chemokine signaling, particularly TNF-α, IL-6, and CCL2, impacting maternal metabolism and fetal programming. While monogenic diabetes (MODY) generally lacks a strong inflammatory signature, emerging evidence suggests that specific subtypes (e.g., HNF1A-MODY) may engage unique cytokine axes. Across complications, including diabetic retinopathy, nephropathy, neuropathy, cardiomyopathy, and macrovascular disease, distinct cytokine/chemokine networks orchestrate fibrosis, leukocyte infiltration, neovascularization, and endothelial dysfunction. Therapeutic interventions targeting these pathways (e.g., IL-1β antagonists, CCR2 inhibitors, IL-17/IL-23 blockade) show promise, yet translation to routine clinical use remains limited by modest efficacy and safety concerns. This review synthesizes current evidence, highlights cytokine/chemokine-driven mechanisms across diabetes forms and complications, and discusses emerging therapeutic strategies and biomarker opportunities for precision medicine. - Source: PubMed
Publication date: 2026/04/08
Lu TinglinQiang WeidongYe Qingqing - Tumor-associated macrophages are pivotal drivers of hepatocellular carcinoma (HCC) progression. However, the functional contributions of proliferating macrophages (Prolif Ms) within the tumor microenvironment (TME) remain poorly defined. - Source: PubMed
Publication date: 2026/04/15
Wang ZengbinXiao RuiyingLiu MengxinCeng LihuaLin ZikunZheng XinyuShi MiaoxinYe HongWu LinqingTang Nanhong - Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a poor prognosis and is easy to developing drug resistance to conventional therapies due to its distinctive tumour microenvironment. Recent advancements have brought attention to the aberrant copper metabolism in this malignancy, but the influence of intracellular cuproplasia and balance on the tumoral immune microenvironment is still uncertain. - Source: PubMed
Publication date: 2026/04/14
Geng RuimanCai HuaweiJi XuxuShen XiaodingWang ZiyaoLi ZhaoLiu RuomengZhang ZhengkunWang DingxueYin ZhaoruZou JiaqiongGuo RongDai PanpanQuan ZhiyouChen LihongKe NengwenLiu Ji - An immunosuppressive tumor microenvironment that facilitates cancer progression is an important challenge in combating the disease. The CCL2-CCR2 axis is a primary facilitator in this process, facilitating the recruitment of CCR2-positive myeloid cells, including M-MDSCs and TAMs, to tumor and metastatic locations. CCR2 is also expressed on tumor cells and regulatory T cells, further enhancing cancer cell motility and immune suppression. Inhibition of this system through genetic deletion or small-molecule inhibitors significantly reduces primary tumor and metastasis in preclinical models, highlighting CCR2 as a promising therapeutic target. Although several CCR2 inhibitors have entered clinical trials, differences in their potency and the limited predictability of murine models have hampered clinical translation. The current work by Sugiyama et al. carefully evaluated 10 human CCR2 antagonists, identifying MK0812 as the most effective inhibitor. Using human CCR2B knock-in mice, they established a practical platform for evaluating CCR2-targeted drugs with direct relevance to human cancer therapy, highlighting the importance of humanized models for translational immuno-oncology. - Source: PubMed
Publication date: 2026/04/14
Chen YanjunShimada Midori - The chemokine network in the microenvironment of pituitary neuroendocrine tumours (PitNETs) may modulate tumour biology, aggressiveness, and treatment responses. We aimed to study the role of various chemokines and chemokine receptors in defining PitNET phenotype and clinical outcomes. We included 96 patients (51 females) with available snap-frozen PitNET tissue from surgery between 2014 and 2020. Chemokine and chemokine receptors were studied by RT-qPCR. Fold difference in mRNA expression was calculated using the ΔΔCt method; chemokine and receptor expression levels were normalised to the expression of the control gene TBP, and expressed relative to a reference sample. Ten chemokines and receptors were studied (CCL2, CCL3, CCL4, CXCL8, CX3CL1, CCR2, CCR4, CCR5, CXCR1, CXCR2), and their expression correlated with clinico-pathological and outcome data, as well as other available microenvironment-related data. We found strong positive correlations between all chemokines and chemokine receptors. Higher chemokine and receptor expression levels were seen in patients who had pituitary apoplexy (CCR2, CXCR1), hypopituitarism at diagnosis (CCL2, CCR4), Ki-67 >3% (CCL4, CXCR2), as well as in patients who required re-operation (CCL3, CXCL8, CXCR2), multimodal therapy (CCL2), and had active disease at last-follow-up (CCL2). There was a positive correlation between the number of pituitary surgeries and expression levels of CCL3, CXCL8, CX3CL1, CXCR1, and CXCR2. Compared to nonfunctioning-PitNETs, somatotropinomas had higher expression of CCL2, CCL4, and CCR2, and lower expression of CX3CL1 and CCR4. Expression of CDH1 (encoding E-cadherin) correlated negatively with CCL2, CCL4, CCR2, CCR4, and CXCR2, while the expression of ZEB1 (mesenchymal marker) positively correlated with CCL3, CCL4, and CX3CL1. PitNETs expressing higher levels of CCL4, CX3CL1, CCR4, CCR5, and CXCR1 had more and bigger vessels. Somatotropinomas treated pre-operatively with somatostatin analogues were associated with higher expression of CCL2, CCR4, CXCR1, and CXCR2, while nonfunctioning-PitNETs pre-surgically treated with dopamine agonists were associated with lower expression of CCL3, CCL4, CX3CL1, CCR5, CXCR1, and CXCR2. Our data suggests that chemokines and chemokine receptors may be involved in the modulation of different tumorigenic mechanisms in PitNETs, including tumour proliferation, epithelial-to-mesenchymal transition, and angiogenesis, and may be associated with more aggressive and difficult-to-treat disease. - Source: PubMed
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