rHu MCP-1
- Known as:
- rHu MCP-1
- Catalog number:
- AK8196-0005
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Akro
- Gene target:
- rHu MCP-1
Related genes to: rHu MCP-1
- 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: rHu MCP-1
Related articles to: rHu MCP-1
- 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
Výmolová BarboraPfeiferová LucieSmetana Tadeáš KarelVýmola PetrTernerová NikolaZubaľ MichalKolář MichalŠáchová JanaGyönyörová SoňaBalážiová EvaHoudová Megová MagdalenaČervenka JakubKupcová Skalníková HelenaŠpanko MichalSmetana KarelLacina LukášNetuka DavidTomáš RobertBušek PetrŠedo Aleksi - Allergic contact dermatitis (ACD) and atopic dermatitis (AD) are driven by distinct T cell programs, and safe long-term topical therapies remain limited. Dermal fibroblasts (dFBs) have emerged as active immunomodulators, but whether they can be therapeutically targeted remains unexplored. - Source: PubMed
Publication date: 2026/07/20
Liu YouxiYin MeimeiYang YichunHeng ShujunZhang WenluSong JinqiuFeng BinxingYang YihanLiu WenjieZhang Ling-Juan