Mouse MCP-1 ELISA kit (4X96T)
- Known as:
- Mouse MCP-1 Enzyme-linked immunosorbent assay test reagent (4X96T)
- Catalog number:
- lf-ek50672
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Mouse MCP-1 ELISA kit (4X96T)
Related genes to: Mouse MCP-1 ELISA kit (4X96T)
- 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: Mouse MCP-1 ELISA kit (4X96T)
Related articles to: Mouse MCP-1 ELISA kit (4X96T)
- Neuropathic pain involves complex neuroimmune interactions across the somatosensory nervous system, yet a comprehensive multi-tissue cellular landscape remains lacking. - Source: PubMed
Publication date: 2026/09/24
Gan XiaofengWang KailongLu DongmingTang HongliangXie JunpingTan LiangyuanPang Jun - Spinal cord injury (SCI) and multiple sclerosis (MS) are distinct central nervous system (CNS) disorders-representing acute traumatic injury and chronic autoimmunity, respectively-yet both feature peripheral immune cell infiltration into the CNS. Here, using human cerebrospinal fluid (CSF) ELISA, public single-cell RNA sequencing datasets, and Ccr2-deficient mouse models of SCI and experimental autoimmune encephalomyelitis (EAE), we conducted a parallel multi-level analysis of the CCL2-CCR2 signaling axis. We found fundamentally distinct temporal dynamics of CCL2: a transient surge during acute SCI, but no significant fluctuation across MS disease stages. Single-cell analysis revealed divergent immune infiltration programs: SCI was dominated by rapid, transient innate immune cell recruitment, while EAE showed sustained accumulation of CD4+ T cells and monocytes. Consistently, CCR2 was acutely induced in infiltrating macrophages in SCI and declined rapidly, but remained persistently elevated in monocytes and CD4+ T cells in EAE. Notably, CCR2 deficiency triggered context-dependent immune remodeling: it reduced macrophage infiltration in SCI with compensatory CD4+ T cell expansion, whereas in EAE it broadly suppressed both innate and adaptive immune infiltration and conferred near-complete disease protection. Collectively, the CCL2-CCR2 axis functions as a context-dependent regulator of immune infiltration, orchestrating transient innate responses in acute injury and sustained adaptive immunity in chronic autoimmunity. These findings highlight the need for disease- and phase-specific targeting of chemokine pathways for precision immunomodulation in CNS disorders. - Source: PubMed
Publication date: 2026/09/28
Zhu XizhongLiao ZikunLiu XiaomingShang ZhizhongWang ZimingLu ZengboLiu BinShu YaqingZhang WeiPang MaoRong Limin - Lung cancer remains the leading cause of cancer-related mortality worldwide, with metastasis, therapeutic resistance, and an immunosuppressive TME representing major barriers to successful treatment. Among the chemokine signaling networks implicated in these processes, the CCL2-CCR2 axis has emerged as an important regulator of tumor progression. By orchestrating the recruitment of monocytes, tumor-associated macrophages, myeloid-derived suppressor cells, and other stromal components, this pathway can establish an immune-permissive niche that supports angiogenesis, epithelial-mesenchymal transition, extracellular-matrix remodeling, metastatic dissemination, and resistance to chemotherapy, targeted therapies, and immunotherapy. Mechanistically, CCL2-CCR2 signaling interacts with key oncogenic pathways, including PI3K/Akt/mTOR, STAT3, NF-κB, Toll-like receptor signaling, and non-coding RNA-mediated networks, thereby amplifying pro-tumor inflammatory circuits within the lung TME. Although accumulating evidence indicates that the axis can exert context-dependent tumor-suppressive effects under specific biological conditions, such as promoting M1 macrophage recruitment or enhancing antitumor immunity in selected settings, its overall contribution in lung cancer appears predominantly tumor-promoting. This review comprehensively summarizes the molecular mechanisms governing CCL2-CCR2 signaling in primary lung cancer and in lung metastases. We further discuss emerging therapeutic strategies directed at this axis, including CCR2 antagonists, CCL2-neutralizing agents, engineered immune-cell approaches, and rational combinations with immune-checkpoint inhibitors and targeted therapies. Collectively, the current evidence provides a strong biological rationale and preliminary translational support for further investigation of the CCL2-CCR2 axis as a potential therapeutic target and exploratory biomarker in advanced lung cancer. However, clinical validation remains limited, and additional well-designed studies are required to determine whether modulation of this pathway can meaningfully improve patient outcomes. - Source: PubMed
Publication date: 2026/09/10
Huang YujieMa JiaBi JianPingPi GuoliangLi YingPeng YiXiao ChuangyingTuo XiulinHan Guang - The mechanisms that cause hypertension remain elusive despite more than a century of investigation. Some of its triggers include aging, sex, salt, diet, stress, experience with adversity, socio-cultural-economic disparities, and poor-quality sleep. The renin-angiotensin-aldosterone and the endothelin systems and other hormones contribute to varying degrees to the rise in BP and target organ damage. It has become increasingly recognized that inflammation and the innate and adaptive immune systems play a role in the etiopathogenesis of hypertension. We review here the participation of different cellular and molecular (genetic and epigenetic) mechanisms that play a role in hypertension via the immune system, including neutrophil extracellular traps, memory T cells, and aldosterone-modulated trained immunity mediated by monocytes/macrophages. Molecular mechanisms, including the effects of neutrophil gelatinase-associated lipocalin as an immunomodulator, and the role of isolevoglandins in mediating oxidative stress-induced activation of the adaptive immune system are analysed. We conclude by summarizing potential therapeutic avenues to address inflammation in hypertension. - Source: PubMed
Publication date: 2026/09/18
Fields EviatarBerillo OlgaSchiffrin Ernesto L - pneumonia triggers a complex, dynamic host response, yet the cellular coordination of inflammation and repair remains poorly defined. - Source: PubMed
Publication date: 2026/09/08
Zong FuliangWang YanHu LingfeiLi LuZhou DongshengZhao JinYang Huiying