Ask about this productRelated genes to: VASH1 antibody
- Gene:
- VASH1 NIH gene
- Name:
- vasohibin 1
- Previous symbol:
- KIAA1036
- Synonyms:
- -
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-21
- Date modifiied:
- 2015-07-22
Related products to: VASH1 antibody
Related articles to: VASH1 antibody
- Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease characterized by chronic inflammation and immune dysregulation, with macrophages playing a critical pathogenic role. However, the molecular determinants underlying macrophage involvement in AAA remain incompletely defined. This study aimed to identify macrophage-related diagnostic biomarkers for AAA through an integrated retrospective analysis of public transcriptomic datasets and experimental validation. - Source: PubMed
Publication date: 2026/02/02
Yang LeiZhou QianZhao GangChen ShanGou WeiHu Zhipeng - IgA nephropathy (IgAN) is the most common primary glomerulonephritis, requiring improved diagnostic tools. We analyzed three cohorts (GSE37460, GSE93798, and GSE115857 are internal validation cohorts) using gene set enrichment analysis on 7751 pathways. A machine learning model was developed and externally validated in multi-cohort gene expression data (external validation cohorts are GSE99339, GSE116626, and GSE104948). Additionally, immunohistochemistry was performed to validate the expression of key biomarkers and the presence of functionally active immune cells. We developed and validated a multi-cohort machine learning diagnostic model. The selected two-step glmBoost + Enet [alpha = 0.4] model achieved high concordance in GSE37460 (κ = 0.704, < 0.001), GSE93798 (κ = 0.486, < 0.001), and GSE115857 (κ = 1.000, < 0.001). Applying the same model to the external validation cohorts demonstrated strong diagnostic accuracy with AUCs of 0.938 (GSE99339), 0.871 (GSE116626), and 0.926 (GSE104948); the corresponding Kappa statistics were κ = 0.699 ( < 0.001), 0.443 ( = 0.018), and 0.615 ( = 0.023). Nine genes were identified as significant for the diagnosis of IgAN, and and emerged as robust biomarkers across the cohorts (all < 0.05). Additionally, immunohistochemistry validation demonstrated a marked increase in HLA-DRA and VASH1 expression in IgAN patients. Immunofluorescence staining indicated a greater presence of CD4 + HLA-DRA+ functionally active/activated CD4+ T cells in IgAN tissues than in controls. This study delivers a reproducible 9-gene machine-learning classifier for precise IgA nephropathy diagnosis and highlights HLA-DRA and VASH1 as promising biomarkers. - Source: PubMed
Publication date: 2026/03/09
Ge YatingJiang XiaoShu JinlianLiu XueqiWu Yonggui - Vasohibin-1 (VASH-1) is an endothelial protein that serves as a negative feedback regulator of angiogenesis. Through its microtubule carboxypeptidase activity, VASH-1 plays a key role in vascular homeostasis. While previous studies have investigated its involvement in vascular regulation, most have focused on isolated functions or specific disease models, without systematically addressing its multi-dimensional regulatory mechanisms, tissue-specific functional paradoxes, and translational potential. This review provides a comprehensive analysis of VASH-1's biological characteristics: its expression is induced by pro-angiogenic factors, and it forms a functional complex with SVBP. In pathological contexts, VASH-1 exhibits paradoxical expression patterns-downregulated in neuroendocrine tumors but upregulated in bladder cancer-and demonstrates tissue-specific functions that either inhibit or promote angiogenesis. Clinically, VASH-1 serves both as a diagnostic marker (e.g., serum biomarker and tissue-based prognostic indicator) and a therapeutic target (such as improving renal disease or promoting tumor vascular normalization). This review aims to elucidate the complex physiological and pathological roles of VASH-1, providing a foundation for future precision intervention strategies targeting VASH-1 in disease diagnosis and therapy. - Source: PubMed
Publication date: 2026/02/09
Wei KekeLi HuiHuang HuiquanBan YinyanLuo XiangbinZhang ChaorenGuo JianTan MinghuaQin Minzhen - Detyrosination is one of the most well-studied post-translational modifications of microtubules (MTs), significantly impacting cell growth, differentiation, division, and intracellular traffic. The VASH1/2-SVBP complex is the first identified carboxypeptidase that specifically catalyzes the detyrosination modification of microtubules. While the structure and mechanisms of the VASH1/2-SVBP complex in mediating this modification are well studied, the regulatory mechanisms governing the catalytic activity of this enzyme remain elusive. Here, we identify a highly conserved five-residue motif located at the C-terminus of VASH1, demonstrating that this motif is crucial for the in vivo detyrosination activity of VASH1. Through peptide pull-down assays combined with mass spectrometry analysis, we identified the chaperone protein HSPA8 as a binding partner of VASH1. The structural model of the HSPA8-VASH1-SVBP ternary complex, predicted by AlphaFold, indicates that HSPA8 interacts with VASH1 through two distinct interaction surfaces. The subsequent biochemical analysis with mutagenesis assays was performed to validate the binding model of HSPA8 to VASH1. Furthermore, in vivo detyrosination assays in HeLa cells reveal that HSPA8 promotes the detyrosination modification of microtubules through direct binding to VASH1. Thus, our study identifies the HSPA8-regulated pathway of microtubule detyrosination, providing a potential target for the diagnosis and therapy of human diseases associated with abnormal microtubule detyrosination. - Source: PubMed
Guo HaoHe LibangWu ZhuoxiYuan RuifangSu HuilingLiu XianchuLi Faxiang - Detyrosination is a reversible posttranslational modification specific to α-tubulin, which has been implicated in cancer progression and invasiveness by promoting epithelial-to-mesenchymal transition. The members of the vasohibin family, VASH1 and VASH2, were previously identified as the first class of enzymes involved in catalyzing this modification. Here, we report the development of a covalent VASH inhibitor, which is characterized by high specificity and low toxicity. By combining the use of a new compound with molecular approaches in lung cancer cell lines, we find that tubulin detyrosination plays an important role in the maintenance of mesenchymal properties. We show that in the absence of VASH activity, collective cell migration and 3D spheroid formation are severely compromised. Moreover, we demonstrate that the observed phenotypes are caused by the accumulation of the important epithelial marker E-cadherin with simultaneous reduction in mesenchymal markers N-cadherin and vimentin. Taken together, our study establishes tubulin detyrosination as a promising target for the future development of anticancer treatment. - Source: PubMed
Publication date: 2025/12/31
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