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
- Glioblastoma (GBM) management is critically impeded by the blood-brain barrier (BBB) and acquired radioresistance. To overcome these hurdles, we engineered a genetically modified biomimetic "nanosponge" (CCR2@VCNPs) designed to synergistically sensitize radiotherapy (RT) and remodel the tumor microenvironment. The nanoplatform consists of a self-assembled core composed of Verteporfin and Celecoxib (VCNPs), which provides high drug loading capacity and enables coordinated delivery of both agents. By cloaking this self-assembled core with macrophage membranes overexpressing CC chemokine receptor 2 (CCR2), the nanoparticles achieve dual-mode targeting: mimicking leukocyte-endothelium interactions for BBB transcytosis and exploiting the CCL2/CCR2 axis for active chemotactic navigation. Notably, the surface CCR2 serves as a "molecular decoy" to intercept RT-induced CCL2, effectively blocking the infiltration of immunosuppressive myeloid cells. Upon tumor accumulation, the self-delivered Verteporfin acts as a potent radiosensitizer by generating singlet oxygen and inhibiting the YAP/TAZ pathway, while Celecoxib (CXB) concurrently abrogates radio-induced immunosuppression by severing the PGE2/COX-2 signaling axis. This integrated strategy promotes robust immunogenic cell death (ICD), effectively transforming the "cold" GBM niche into a "hot" immunological phenotype. In orthotopic GBM mouse models, CCR2@VCNPs significantly prolonged median survival and suppressed tumor recurrence. By integrating molecular self-assembly with genetic membrane engineering, offers a comprehensive solution to therapeutic resistance and holds great promise for clinical GBM management. - Source: PubMed
Publication date: 2026/07/02
Liu XinyingHao XinyanLiu JiayiTang TiantianLiao DehuaHan RuyueTang YuchengGuo MengenHuang HaiPeng YanjinXiang DaxiongWang MingWu Junyong - Immune-inflammatory cascade is a dominant process mediating allograft inflammatory injury and rejection, thereby threatening the survival of both allografts and recipients. However, the primary driver of this progression remains unclear, and targeted intervention remains a critical challenge in the development of effective treatments. - Source: PubMed
Publication date: 2026/07/01
Yi XuewenMeng ChaoyangZhang HuipengLu QianrangZhang KeLi XinqiangHuang HaitaoJiang JingyuLin YimouXing MuqiongChen HuiKong GangchengZhang XiaogeXu YiranFang JunZheng ShusenLi HaoLi HongjunGu ZhenLing Qi - Peritoneal metastasis is a major contributor to progression, recurrence, and treatment failure in epithelial ovarian cancer (EOC) and is closely associated with dynamic remodeling of the peritoneal tumor microenvironment (TME). Interactions among tumor cells, ascites, the omental niche, stromal components, and immune cells collectively shape metastatic dissemination and therapeutic response. CC chemokines are important regulators of these processes, linking immune-cell trafficking with tumor-cell plasticity, metabolic adaptation, angiogenesis, and therapy resistance. This review summarizes the roles of CC chemokines in EOC progression within a chemokine-driven peritoneal niche remodeling framework encompassing four key stages: early dissemination, survival in ascites, omental colonization, and therapy resistance. Among the major signaling axes, CCL2-CCR2 is primarily associated with monocyte recruitment and myeloid-dominant immunosuppression, whereas CCL5-CCR5 is linked to stromal immune regulation and cancer stem-like phenotypes. Additional pathways, including CCL18, CCL20-CCR6, CCL22-CCR4, and CCL1-CCR8, contribute to T-regulatory cell recruitment, immune suppression, and hypoxia-associated responses. The review further discusses the limited efficacy of chemokine-targeted monotherapy, highlighting challenges posed by signaling redundancy, compensatory pathways, spatial heterogeneity, and insufficient biomarker-guided patient selection. Recent advances in single-cell and spatial transcriptomic technologies have improved the characterization of compartment-specific chemokine programs within the EOC microenvironment. Finally, emerging combination strategies involving chemokine blockade together with immune checkpoint inhibitors, metabolic interventions, PARP inhibitors, and ferroptosis-related approaches are evaluated. However, successful clinical translation will require precise patient stratification, effective toxicity management, and validation in clinically annotated cohorts. - Source: PubMed
Publication date: 2026/06/30
Xu BingYao JinhanHan MengruZhang Yuquan - Chronic stress is associated with poor prognosis in colorectal cancer (CRC), but the underlying immune mechanisms remain poorly defined. This study investigates how β-adrenergic signaling, a key component of the stress response, modulates the tumor microenvironment. We demonstrate that stressed CRC patients have elevated serum CCL2, and high tumoral expression of CCL2 and its receptor CCR2 predicts poor survival. Single-cell analysis reveals that within the tumor microenvironment of colorectal cancer, macrophages constitute the primary subset of immune cells responsible for CCL2 secretion. Mechanistically, we demonstrate that stimulating macrophages with isoproterenol, a well-established in vitro method to mimic chronic stress signaling, induces their polarization toward an M2-like phenotype and significantly increases CCL2 secretion. Functionally, conditioned media from these "stressed" macrophages enhanced CRC cell proliferation and invasion in a CCR2-dependent manner, an effect abrogated by pharmacological CCR2 blockade. Collectively, our findings pinpoint the CCL2-CCR2 pathway as the central mediator of a 'stress-macrophage-tumor' axis, validating it as a key therapeutic target to intercept CRC progression driven by a chronic stress state elicited by β-adrenergic activation. - Source: PubMed
Publication date: 2026/06/25
Wang MengyunPang JiayuWang WenbinXu QianLu YanjieZuo YanzhenLi YuHong - This study evaluated the diagnostic value of C-C motif chemokine ligand 2 (CCL2) and C-C chemokine receptor type 2 (CCR2) in pleural effusions for distinguishing histological subtypes of lung cancer (LC). - Source: PubMed
Publication date: 2026/06/28
Yu JieHuang YongChen Weirong