Human Azurocidin 1 ELISA , AZU1
- Known as:
- Human Azurocidin 1 Enzyme-linked immunosorbent assay test , AZU1
- Catalog number:
- E01A0474
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Azurocidin 1 ELISA AZU1
Related genes to: Human Azurocidin 1 ELISA , AZU1
- Gene:
- AZU1 NIH gene
- Name:
- azurocidin 1
- Previous symbol:
- -
- Synonyms:
- AZU, CAP37, AZAMP, HBP, NAZC, HUMAZUR
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-21
- Date modifiied:
- 2014-11-18
Related products to: Human Azurocidin 1 ELISA , AZU1
Related articles to: Human Azurocidin 1 ELISA , AZU1
- Neutrophil extracellular traps (NETs) play crucial roles in cancer progression, but their regulatory mechanisms in breast cancer remain poorly understood. We developed a NETs-related prognostic risk model using TCGA breast cancer data and identified key biomarkers through bioinformatics analysis. AZU1 expression was validated in clinical samples using qRT-PCR and immunohistochemistry. In vitro experiments investigated AZU1's effects on neutrophil activation and NET formation using recombinant protein treatment, co-culture assays, and flow cytometry. Mechanistic studies employed phospholipase C (PLC) inhibition and PAD4 knockdown approaches. An orthotopic mouse model validated in vivo findings. Four NETs-related genes (F2RL2, AZU1, IL33, ELANE) constituted a robust prognostic model with good predictive performance. AZU1 showed significant upregulation in breast cancer tissues and correlated with advanced tumor stages. AZU1 overexpression in breast cancer cells enhanced neutrophil recruitment and NET formation through PLC signaling activation. Recombinant AZU1 dose-dependently activated neutrophils, promoted NET formation, and enhanced cancer cell invasion via epithelial-mesenchymal transition induction. PLC inhibition and PAD4 knockdown effectively blocked AZU1-induced neutrophil activation. In vivo experiments confirmed that AZU1 overexpression accelerated tumor growth and metastasis, while PAD4 inhibition reversed these effects. AZU1 promotes breast cancer progression through PAD4-dependent NET formation, representing a potential therapeutic target for breast cancer treatment. - Source: PubMed
Publication date: 2026/08/01
Huang ZhenWu ZheZhu GuiyueQiu FangyuLi LihuiXie YujieWei ChunyuPan YinhuaZou QuanqingTang Yuntian - This study aimed to identify candidate shared transcriptomic signals between major depressive disorder and dermatomyositis through an integrative bioinformatic reanalysis of public GEO datasets with single-cell contextualization. The analytical workflow included Weighted Gene Co-expression Network Analysis (WGCNA) for key module identification, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses for functional characterization, GeneMANIA- and a network visualization platform-based network analysis for candidate-gene prioritization, and evaluation of 113 machine-learning models combined with SHapley Additive exPlanations (SHAP) for diagnostic feature selection. Gene Set Enrichment Analysis (GSEA), immune infiltration analysis, and single-cell RNA-seq-based contextualization were subsequently performed to further characterize the immune-related cellular context of the identified signals. Integration of dermatomyositis-related GEO datasets identified 570 differentially expressed genes, from which 33 candidate shared genes were obtained via WGCNA. Functional enrichment and network analyses highlighted immune defense, cytotoxicity, and pathways including PPAR, IL-17, and antigen processing, with ELANE, PPBP, and CTSG emerging as highly connected nodes. Machine-learning-based feature prioritization retained 8 candidate model-selected genes, namely KIF4A, OLR1, KIR2DL4, KRT23, KIR3DS1, AZU1, SCG5, and LRRC37E. Immune infiltration analysis associated these shared genes with regulatory T cells (Tregs), resting mast cells, resting dendritic cells, and both classically activated (M1) and alternatively activated (M2) macrophages. Single-cell RNA-seq contextualization further suggested that CD8⁺ T-cell subsets with different candidate-gene score states showed distinct intercellular communication patterns. Among these, the MIF-(CD74+CD44) axis and signals from naive/central memory T cells were notable features requiring further validation. Overall, this study identified candidate shared transcriptomic signals between major depressive disorder and dermatomyositis and highlighted immune-related cellular contexts that warrant further validation in true comorbid cohorts. - Source: PubMed
Publication date: 2026/06/26
Teng FeiZheng SisiZhang XiatianLu ZhongwenWang PengruiWang PengYin Dongqing - The contribution of human genetics in shaping the abundance of gut microbiota is small, about 5%; however, it can inform about disease etiopathogenesis, including multiple sclerosis (MS). Searching for MS-gut microbiota cross-comparison of reported genome-wide association studies (GWAS), we identified a coincident association of the disease with a commensal - Akkermansia massiliensis-in the selective Fc receptor of secretory IgA gene (FcRL3). Those two signals colocalized, supporting that lower abundance of A.massiliensis may contribute to MS predisposition. In cis, the FcRL3-MS predisposing signal downregulates the FcRL3 protein production and modulates the dynamic intron usage between naïve and mature B-cells, which we believe to be the primary molecular mechanism associated with MS risk in this region. The signal also increases the expression of the FcRL5 gene. In trans, it reduces the expression of neuropeptide B/W receptor 1 (NPBWR1) and azurocidin (AZU1), whereas it increases the expression of the tumor necrosis factor receptor superfamily, member 13B (TACI). Our view of MS etiopathogenesis suggests that low levels of FcRL3 and A. massiliensis may predispose to MS by causing impaired self-tolerance to commensal microbiota, dysregulation of B-cell function, and immune system effects on the neuroendocrine signaling by AZU1 and NPBWR1 proteins, which may be further investigated as targets for MS. - Source: PubMed
Publication date: 2026/07/11
Orrù ValeriaMarongiu MicheleCocco EleonoraZoledziewska Magdalena - Heparin-binding protein (HBP) is an inflammatory protein released by activated polymorphonuclear white cells. It has been suggested as a predictor of sepsis progression and organ dysfunction and plays a role in the pathophysiology of endothelial dysfunction. Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor with pro-inflammatory effects, and high levels are found in patients with sepsis and acute respiratory distress syndrome. We investigated HBP and ET-1 plasma levels in critical COVID-19 disease with the aim of evaluating whether they were associated with 60-day mortality or the need for invasive mechanical ventilation (IMV). These levels were compared with those of a cohort of post-trauma intensive care unit (ICU) patients. - Source: PubMed
Publication date: 2026/06/23
Halldorsdottir HallaEriksson JesperRooyackers OlavGrip JonathanMårtensson JohanWeitzberg EddieOldner Anders - To investigate the correlation between serum heparin-binding protein (HBP) and other clinical indicators with the bronchoscopic lesion severity in children with pneumonia (MPP), in order to understand their potential value in guiding diagnosis and treatment. - Source: PubMed
Li Yu-RongZhang Cui-LingWu YiLiu RuMeng Ling-Jian