rHu MCP-1
- Known as:
- rHu MCP-1
- Catalog number:
- AK8196-1000
- Product Quantity:
- 1mg
- 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
- This review examines the impact of genetic variation in chemokines and their receptors on the risk of atherosclerosis and adverse cardiovascular outcomes. - Source: PubMed
Publication date: 2026/03/13
Zangas PanagiotisGeorgakis Marios K - Elderly bronchial asthma is a heterogeneous, often non-atopic disorder characterized by airway inflammation and remodeling influenced by age-related immune dysregulation. This review aims to elucidate the roles of helper T cells (Th cells) and chemokine networks in driving elderly asthma and to emphasize implications for precise diagnosis and targeted therapy. We performed a narrative synthesis of studies from PubMed and Web of Science (January 2020-December 2025) utilizing the keywords "elderly asthma," "helper T cells," "chemokines," "airway inflammation," and "immunosenescence," focusing on human cohorts aged ≥65 years and aged animal models. The literature reveals that the pathogenesis of elderly asthma is characterized by an imbalance between T helper 1 (Th1) and T helper 2 (Th2) responses, enhanced T helper 17 (Th17) activity, and diminished regulatory T cell (Treg) function, changes that are exacerbated by immunosenescence. Key chemokine axes-including C-C motif chemokine ligand 11 (CCL11)/C-C chemokine receptor 3 (CCR3), C-X-C motif chemokine ligand 8 (CXCL8)/C-X-C chemokine receptor 1 (CXCR1) and C-X-C chemokine receptor 2 (CXCR2), C-C motif chemokine ligand 2 (CCL2)/C-C chemokine receptor 2 (CCR2), C-X3-C motif chemokine ligand 1 (CX3CL1)/C-X3-C chemokine receptor 1 (CX3CR1), and stromal cell-derived factor 1 (SDF-1)/C-X-C motif chemokine ligand 12 (CXCL12)/C-X-C chemokine receptor 4 (CXCR4)-facilitate the recruitment of eosinophils, neutrophils, and monocytes/macrophages, thereby sustaining airway inflammation and remodeling. Overall, Th-chemokine circuits represent actionable targets for biomarker-guided, personalized treatment; however, further mechanistic and clinical validation studies specific to the elderly population are crucial for effective translation into practice. - Source: PubMed
Publication date: 2026/03/10
Wu Youhua - The CCR2/CCL2 molecular axis is a critical mediator of abdominal aortic aneurysm (AAA) pathogenesis. It has been demonstrated to drive chronic inflammation, extracellular matrix degradation, and vascular remodeling through the recruitment and activation of monocytes/macrophages and other immune cell types. Pre-clinical studies demonstrate that CCR2 inhibition reduces AAA formation, expansion, and progression in animal models. Emerging imaging techniques have validated CCR2 as a biomarker for AAA instability in humans. Although clinical trials targeting CCR2 are currently limited in number, ongoing translational studies highlight that CCR2 blockade is a promising therapeutic strategy to mitigate AAA expansion and the risk of rupture. This review underscores the potential of CCR2-targeting interventions to fill a critical unmet need to develop effective medical therapies for longitudinal clinical AAA management. - Source: PubMed
Publication date: 2026/02/17
Wahidi RyanElizondo-Benedetto SantiagoCatlett RyanKoklu BeraZayed Mohamed A - This research evaluated the potential mechanisms of ASX on EIMD. The network pharmacology, machine learning, and transcription sequencing were applied to explore the targets of ASX improving EIMD, which were then validated by molecular dynamics simulation and experiments. Twenty five key targets were screened after topological network analysis and mainly enriched in the Toll-like receptor signaling pathway, NF-κB signaling pathway, and Cytokine-cytokine receptor interaction. Through machine learning algorithms, four candidate targets, including CCL2, NFE2L2, TLR4, and TGFB1, were acquired. Combined with transcriptome sequencing results, CCL2 and TLR4 were finally identified as core targets for ASX to improve EIMD. Molecular dynamics simulation confirmed the strong binding affinity of ASX-CCL2 and ASX-TLR4 complexes. Besides, RT-PCR and Western blot revealed that the mRNA and protein expression of the TLR4/MyD88/NF-κB/CCL2/CCR2 pathway in the EIMD model were significantly down-regulated after ASX intervention. ASX might effectively attenuate muscle damage during exercise through the TLR4/MyD88/NF-κB/CCL2/CCR2 pathway. - Source: PubMed
Publication date: 2026/01/14
Wang JiayiBi XiangyuWang YefanWu Lijun - Advances in multimodal therapy for high-risk neuroblastomas (NBs) have plateaued, prompting therapeutic initiatives to harness the immune system. NBs, however, are immunologically "cold" and a significant challenge to immunotherapy. Here, in a Jurkat lymphocyte cytotoxicity model, we describe an antigen-independent, cell-mediated mechanism for eliminating NB cells, first detected in PMA-activated low pcDNA-SH-SY5Y and high TrkAIII-SH-SY5Y TrkAIII-expressing cells, which are resistant to Jurkat elimination under normal conditions. Characterization of this mechanism through live cell imaging, adhesion assays, RT-PCR, Western blotting and indirect IF, employing a variety of inhibitors, indicates that it initiates with PMA-induced NB cell CCL2 expression. This results in CCL2 promotion of Jurkat CCR2b expression, CCL2/CCR2b-mediated Jurkat LFA-1 activation and the formation of cytotoxic lipid-raft LFA1/ICAM-1 immune synapses, through which Jurkat m-TRAIL combines with PMA-enhanced NB cell DR5/TRAIL-R2 expression to induce NB cell apoptosis. This mechanism is enhanced by the NB-associated oncoprotein TrkAIII through Shp/Src-regulated c-FLIP sequester and is PD-L1/PD-1-independent and resistant to osteoprotegerin. It eliminates both non--amplified (SH-SY5Y and SK-N-SH) and -amplified (SMS-KCNR) NB cells that exhibit PMA-inducible CCL2 expression but not -amplified NB cells (IMR-32 and NB-1) that exhibit CCL2 repression, and is offset by reciprocal NB cell-induced Fas-mediated Jurkat cell apoptosis. These findings form a solid foundation for further pre-clinical development aimed at identifying clinically relevant physiological immune cell equivalents and alternative PKC activators, with the ultimate goal of translating this mechanism into an effective immune-therapeutic approach for the treatment of high-risk non-immunogenic NBs, especially NBs that exhibit CCL2 and TrkAIII expression. - Source: PubMed
Publication date: 2026/02/18
Sbaffone MaddalenaMartelli IlariaCipriani PaolaFarina Antonietta RosellaCappabianca Lucia AnnamariaMackay Andrew Reay