MCP 1
- Known as:
- MCP_1
- Catalog number:
- CHM-271
- Product Quantity:
- 5µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- MCP_1
Related genes to: 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: MCP 1
Related articles to: MCP 1
- To find the association between serum levels of inflammatory cytokines (CCL2, CCR2, XCL1, and IFN-γ) and normotension, hypertension, and hypertensive heart disease, and to explore whether combined cytokine profiles differ across the defined groups. - Source: PubMed
Sahito Falak SeharYasmeen GhazalaFarman Muhammad Tariq - Chronic pain affects hundreds of millions worldwide, yet current treatments-from NSAIDs to opioids-fall short and bring unwanted side effects. Neuroinflammation drives bidirectional glial-neuronal communication, a core mechanism underlying central sensitization in chronic pain, with chemokines serving as key mediators. Most studies to date have zeroed in on isolated pathways or specific anatomical sites, missing the bigger picture. We pull together findings across the neural axis, spanning peripheral sensory ganglia, the spinal dorsal horn, and higher brain centers, then dissect the molecular machinery of chemokine-mediated crosstalk among microglia, astrocytes, and neurons. We trace downstream regulatory cascades through two major axes-CCL2/CCR2 and CX3CL1/CX3CR1-along with their effector branches (ERK-GluN2B, p38 MAPK-NF-κB), map out polarization phenotypes (M1/M2 for microglia, A1/A2 for astrocytes), and detail the functional shifts glia undergo in disease states. By knitting scattered observations into a unified regulatory map of chemokine signaling across the chronic pain neural network, this review addresses the field's persistent lack of systematic integration. - Source: PubMed
Publication date: 2026/05/01
Fan MingyuanLiang ZhiShen JiayiYang HuiZhao LipingLi MinZheng Jie - To explore the molecular mechanisms underlying cystoid macular edema (CME) through protein-protein interaction (PPI) network analysis, identifying key regulatory proteins, functional modules, and enriched biological pathways relevant to its pathogenesis. - Source: PubMed
Shariati Mehrdad Motamed - Atherosclerotic plaque destabilization is promoted by inflammatory cell recruitment, tissue cell death, and mechanical weakening. Neutrophils drive vascular tissue injury and perpetuate inflammation and represent a viable therapeutic opportunity. Here, we identify a distinct subset of activated neutrophils within atherosclerotic lesions that express the chemokine receptor CCR2 (C-C chemokine receptor type 2), which directs their migration toward areas enriched with smooth muscle cells and contributes to plaque instability. - Source: PubMed
Publication date: 2026/05/14
Farjia MeriemePan ChangBraster QuinteLemnitzer PatriciaSachs NadjaVöcking Lina-MarieChevre RaphaelMalamud MarianoSchulz ChristianMaegdefesel LarsSoehnlein OliverSilvestre-Roig Carlos - Metabolic-dysfunction-associated steatotic liver disease (MASLD) is a major chronic liver disorder that progresses through inflammation and fibrosis to cirrhosis, yet no effective pharmacological therapy is available. Extracellular vesicles (EVs), which are key mediators of intercellular communication, have recently been reported to exert preventative and therapeutic effects in disease models. This study evaluated the oral efficacy of EVs derived from the microalga (CEVs) in an MASLD mouse model. Male C57BL/6J mice were assigned to a control group (normal diet), an MASLD group (choline- and methionine-deficient high-fat diet; CDHF), or CEV group (CDHF + CEVs). Twelve-week CEV administration did not alter the CDHF-induced reduction in circulating lipid levels or produce an increase in hepatic lipid content. However, CEV treatment significantly suppressed CDHF-induced fibrosis with collagen accumulation and reduced the mRNA expression of fibrosis-related genes, including , , , and . CEVs also significantly downregulated the expression of macrophage-derived inflammatory mediators-, , and -and reduced lobular inflammatory foci. These findings suggest that CEVs attenuate hepatic fibrosis by modulating early inflammation associated with steatosis and inhibiting hepatic stellate cell activation. This study supports the potential of CEVs as a novel oral intervention for slowing MASLD progression. - Source: PubMed
Publication date: 2026/04/22
Harada HinataOhsaki YusukeAgista Afifah ZahraHo Hsin-JungHirose TakuoYamada KotaroFurukawa MutsumiNochi TomonoriChiu Wan-ChunChen Ya-LingYeh Chiu-LiYang Suh-ChingMori TakefumiShirakawa Hitoshi