CXCL16 Antibody
- Known as:
- CXCL16 Antibody
- Catalog number:
- XW-7727
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CXCL16 Antibody
Related genes to: CXCL16 Antibody
- Gene:
- CXCL16 NIH gene
- Name:
- C-X-C motif chemokine ligand 16
- Previous symbol:
- -
- Synonyms:
- SR-PSOX, CXCLG16, SRPSOX
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-21
- Date modifiied:
- 2016-10-05
Related products to: CXCL16 Antibody
Related articles to: CXCL16 Antibody
- Peritoneal fibrosis, driven by M2 macrophage polarization, limits the long-term application of peritoneal dialysis (PD). Although ADAM19 is known to mediate fibrosis in other organs, its specific role in PD-associated peritoneal fibrosis remains unclear. PD patients were enrolled in a single center and divided into three groups depending on the PD time. Demographic and clinical data were collected. We detected the expressions of ADAM19, Notch1, Fibrosis-associated protein, chemokines and inflammatory factors in the peritoneum dialysis effluent by real-time PCR and western-blot assays. Macrophages were identified through flow cytometry. Then we analysis the relationship between ADAM19 and clinical data in PD patients. Furthermore, we established mouse models for peritoneal fibrosis to verify the biological function of ADAM19 in regulating macrophage polarization. In the long-term group, the fibrotic proteins (Fibronectin, α-SMA) and inflammatory factors (IL-6, IL-10) and chemokines (CCL5, CCL2, CXCL16) were higher than short-term group and more macrophages polarized towards M2. ADAM19 expression was linearly correlated with dialysis time and Kt/v. The AUROC of ADAM19 was 0.738 to identify the predictive value for peritoneal dialysis adequacy. The cut-off of ADAM19 RNA level was 7.84. In logistic regression models, higher ADAM19 (≥ 7.84) was also independently associated with lower Kt/v (< 1.67). Additionally, the results revealed a moderate increment of M1 macrophage (CD86+) and enormous rise of M2 macrophage (CD206+) with high-glucose dialysis fluid in mice model. Furthermore, the 8-week G4.25% group showed significant growth of M2 macrophage compared to the 4-week G4.25% group, indicating that prolonged dialysis duration has a more pronounced effect on promoting M2 polarization of macrophages via ADAM19/Notch1 signaling pathway. Through stimulating chemokines and inflammatory factors, ADAM19 regulated macrophage polarization and was correlated to the progression of peritoneal fibrosis. ADAM19 is expected to be a novel indicator for detecting peritoneal ultrafiltration function in PD patients. - Source: PubMed
Publication date: 2026/05/02
Xu KunyueYu JinHe MinhuiJiang XueYuan Yuan - Chemotherapy for peritoneal metastases (PM) is severely constrained by the limited intratumor drug penetration and insufficient retention within tumors. Herein, we rationally engineer a fibroblast activation protein (FAP)-triggered transformable nanoassembly of peptide-drug conjugate to address these bottlenecks for PM chemotherapy. We identify 7-ethyl-10-hydroxy-camptothecin (SN38) as the preferred cytotoxic agent and C-X-C motif chemokine ligand 16 (CXCL16)-mimic peptide as the selected tumor-penetrating peptide, which are conjugated via a FAP/glutathione-dual responsive linker to form a SN38-STPC conjugate. SN38-STPC is further assembled with pre-screened 1,2-dimyristoyl-sn-glycero-3-phosphoethanolamine-N-[methoxy(polyethylene glycol) 1000] (DMPE-PEG) to construct transformable nanoassemblies (SN38-STPC NA). SN38-STPC NA undergoes FAP-triggered transformation into nanofibers and GSH-responsive drug release. Both in murine CT26 PM model and patient-derived xenograft (PDX)-PM model, SN38-STPC NA achieves efficient intratumor penetration and prolonged retention in PM lesions, causing notable inhibition of PM progression. Especially in PDX-PM model, SN38-STPC NA reduces PM tumor weight by 80.9%, decreases PM nodule number by 82.3%, and extends median survival by 1.76-fold, outperforming the clinical standard FOLFIRI regimen. Collectively, the transformable SN38-STPC NA represents an encouraging delivery platform for effective PM chemotherapy. - Source: PubMed
Publication date: 2026/04/30
Lu YiChi YifeiCao SiyuweiNie WeiminZhang YichenWang ShuaiHuang MingxuanLiang YiyuWu YaoWu JingboWang RenjieHuang MinTan WenfuGeng MeiyuZhang Zhiwen - ObjectiveThis study aimed to identify immune-related hub genes shared between acute myocardial infarction (AMI) and metabolic syndrome (MetS), and to construct and validate a blood-based gene diagnostic signature for AMI, with the hypothesis that this signature may be informative for AMI risk assessment in MetS patients.MethodsTwo AMI datasets (GSE66360, GSE61145) and one MetS dataset (GSE98895) were obtained from the Gene Expression Omnibus (GEO) database. Based on the GSE66360 dataset, 285 AMI-related common genes were identified as the intersection between 1409 differentially expressed genes (DEGs) and 304 module genes, identified via Limma and weighted gene co-expression network analysis (WGCNA), respectively. Subsequently, the intersection of these 285 AMI-related common genes and 1446 MetS-related DEGs yielded 40 genes that were primarily associated with immunoregulation, as revealed by functional enrichment analysis. After constructing a protein-protein interaction (PPI) network, 30 node genes were selected and ranked according to node degree. Six candidate hub genes (THBD, MMP9, IRAK3, CXCL16, NLRP3, and JDP2) identified via machine learning were used to establish a diagnostic model and evaluate its diagnostic value.ResultsWe revealed that the six candidate genes demonstrated strong diagnostic value for AMI (AUC ranging from 0.86 to 0.94, with 95% confidence intervals [CIs]). Moreover, a diagnostic nomogram constructed from these genes allows for visual quantification of AMI probability. Immune cell infiltration analysis revealed dysregulation across multiple immune cell subsets in AMI. These six immune-based hub genes have been identified as potential diagnostic biomarkers for AMI, with hypothesized relevance in MetS patients.ConclusionsThese findings provide a hypothesis-generating resource for understanding inflammatory links between MetS and AMI, though clinical utility for risk stratification in MetS patients requires further prospective validation. - Source: PubMed
Publication date: 2026/04/28
Feng NiFeng MeiguoRuan JianZhou CaiSong XiaoyingChen LiHou Shuai - Tumor-associated macrophages (TAMs) are pivotal in the immunosuppressive tumor microenvironment of pancreatic ductal adenocarcinoma (PDAC). The efficacy of targeting the CSF-1/CSF-1R axis in PDAC remains uncertain. Using single-cell RNA sequencing on specimens from patients treated with Surufatinib plus chemotherapy, we identified a distinct subset of damage-associated macrophages (DAMs) characterized by high GPR34 expression. In Gpr34 mouse models and in vitro co-cultures, GPR34 macrophages responded to tissue damage by releasing lysophosphatidylserine (LysoPS), which enhanced CXCL16 secretion and efferocytosis. This efferocytosis promoted MHC-I degradation via the macrophage lysosomal pathway, leading to CD8 T cell exhaustion. Combining a GPR34 antagonist with chemotherapy and surufatinib significantly enhanced anti-tumor responses in preclinical models. These findings identify GPR34 as a promising immune therapeutic target. - Source: PubMed
Publication date: 2026/04/28
Guo XiaofanLiu YuxiaoLi TianchenAn XiaopengSong YuningXu PeijunHuang JingZou YipingXu BohangXie YongjieLi ZekunMeng ChenyangZhao TiansuoWang XiuchaoWang HongweiGao ChuntaoZhou XuanYu JunGao SongHao Jihui - Endothelial dysfunction profoundly compromises the barrier function that precludes trans-endothelial entry of low-density lipoprotein cholesterol (LDL-C) into the vessel wall. LDL-C retention in the vessel wall is atherogenic and its flux involves several mechanisms including LDL-receptor (LDL-R) mediated transcytosis, a process that is facilitated by inflammatory stressors. In this study, we aimed to investigate the role of interleukin-6 (IL-6) in regulating LDL-R and LDL-C uptake by vascular endothelial cells. - Source: PubMed
Publication date: 2026/04/25
Zegeye Mulugeta MVeettil Jishamol TParamel Geena VKurt SetaSalihovic SamiraLjungberg Liza UKumawat Ashok KSirsjö Allan