Human CX3CL1 ELISA Kit
- Known as:
- Human CX3CL1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 55r-1577
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- Human CX3CL1 ELISA Kit
Related genes to: Human CX3CL1 ELISA Kit
- Gene:
- CX3CL1 NIH gene
- Name:
- C-X3-C motif chemokine ligand 1
- Previous symbol:
- SCYD1
- Synonyms:
- NTN, C3Xkine, ABCD-3, CXC3C, CXC3, fractalkine, neurotactin
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2016-10-05
Related products to: Human CX3CL1 ELISA Kit
Related articles to: Human CX3CL1 ELISA Kit
- Epithelial ovarian cancer (EOC) is characterized by aggressive peritoneal dissemination and an immunosuppressive tumor microenvironment in which tumor-associated macrophages (TAMs) play a central role. Chemokine signaling pathways regulate macrophage recruitment and function; however, the contribution of the CX3CL1-CX3CR1 axis to ovarian cancer progression and TAM-mediated effector mechanisms remains unclarified. This study aimed to clarify the role of CX3CL1-CX3CR1 signaling in ovarian cancer progression, focusing on macrophage-derived pro-tumorigenic factors. CX3CL1 and CX3CR1 expression was examined in human EOC and healthy ovarian tissues by real-time polymerase chain reaction and immunohistochemistry. Functional effects of CX3CL1 on ovarian cancer cells were evaluated via migration and proliferation assays in the murine ID8 cell line. An intraperitoneal syngeneic ovarian cancer model was established by injecting ID8 cells into wild-type and Cx3cr1-deficient mice. Tumor burden, ascites formation, survival, macrophage infiltration, and expression levels of matrix metalloprotease-2 (MMP-2) and transforming growth factor-β (TGF-β) were assessed by histological, immunohistochemical, and molecular analyses. CX3CL1 and CX3CR1 expression was significantly upregulated in human EOC tissues and associated with marked macrophage infiltration. CX3CL1 stimulation enhanced migration, but not proliferation, of ID8 cells. Cx3cr1 deficiency significantly suppressed intraperitoneal tumor growth, reduced ascitic fluid volume, and prolonged survival. This was accompanied by reduced CX3CR1 TAM accumulation and decreased MMP-2 and TGF-β expression, which were predominantly produced by infiltrating macrophages. The CX3CL1-CX3CR1 axis promotes ovarian cancer progression by recruiting MMP-2- and TGF-β-producing macrophages. Targeting CX3CR1-dependent TAM functions may represent a therapeutic strategy for limiting peritoneal dissemination in ovarian cancer. - Source: PubMed
Publication date: 2026/06/05
Tanizaki-Horiuchi YukoIshida YukoKobayashi AyaYahata TamakiKuninaka YumiToujima SaoriNosaka MizuhoMatsuki ReikoKimura AkihikoMizoguchi MikaMukaida NaofumiIno KazuhikoKondo Toshikazu - Schizophrenia pathogenesis may involve aberrant synaptic pruning mediated by excessive complement system activity (CSA) and altered microglial function. Microglia and CSA are tightly regulated by neuro-immune regulators (NIREGs) which regulate adverse innate response and play a critical role in the regulation of the synaptic pruning process. This study investigated transcriptional alterations of NIREGs in the brain and blood tissues of individuals living with schizophrenia (SZ individuals) vs. healthy controls (HC). - Source: PubMed
Publication date: 2026/06/11
Boughanmi Mohamed-ElMehdiLespine Louis-FerdinandLeboyer MarionDemily CarolineRey Romain - Preterm infants encounter DEHP through medical devices and equipment. While hyperoxia is known to promote cardiac remodeling and dysfunction, the impact of early phthalate exposure is understudied. We hypothesized that independent and combined DEHP and hyperoxia exposure would impair neonatal cardiovascular development. - Source: PubMed
Publication date: 2026/06/10
Toor FatimaSargsyan ManeAkselrod AbigailZhao ChunfangSen NamitaNasim MansoorStroustrup AnnemariePerveen Shahana - Vascular cognitive impairment (VCI) is a syndrome of cognitive dysfunction attributable to vascular risk factors and cerebrovascular diseases, representing a major component of global dementia burden. Dysglycemia, encompassing diabetes mellitus and impaired glucose regulation, is increasingly recognized as a modifiable risk factor for cognitive decline, particularly VCI. Chronic low-grade inflammation mediates the association between metabolic dysfunction and neurodegeneration. The lack of validated diagnostic tools for early VCI detection in high-risk dysglycemic populations highlights the urgent need for robust diagnostic models based on molecular signatures. - Source: PubMed
Publication date: 2026/05/22
Wang YuyingZhao ZhenyuJi LinnaHe HaoyingPeng SisiXu JuanXu ZhipengZhang Junjian - In the context of muscle loss, bone repair is impaired, suggesting that muscle derived signals contribute to bone regeneration. However, how muscle surrounding the injury site communicates with the bone repair niche remains unclear. Here we found that CX3CL1 expression was induced in endothelial cells in muscle surrounding a femoral bone injury site. Deletion of impaired bone healing, demonstrating a functional role for CX3CL1 in bone repair. A CX3CL1 receptor, CX3CR1, was expressed by PDGFRα⁺ stromal progenitors and lineage tracing showed that CX3CR1 expressing osteoprogenitor lineage cells accumulated at the injury site during repair. PDGFRα⁺ stromal progenitors showed enhanced osteoblastogenesis in response to recombinant CX3CL1. In older mice, local CX3CL1 delivery increased PDGFRα⁺CX3CR1⁺ osteoprogenitor accumulation and improved bone repair. These findings identify a muscle bone signaling pathway in which endothelial CX3CL1 promotes bone repair through CX3CR1 expressing osteoprogenitors. - Source: PubMed
Publication date: 2026/05/27
Ishikawa KojiMarius ChoiselleShimada EijiroNadesan PuviNguyen TuyetIshikawa MahokoHoque JiaulMa XinyiNakagawa MakotoAllen NicholasAbe KokiVarnadore PhilipSouma TomokazuVarghese ShyniYahara YasuhitoPuviindran VijithaAlman Benjamin Aaron