Ask about this productRelated genes to: VNN1 antibody
- Gene:
- VNN1 NIH gene
- Name:
- vanin 1
- Previous symbol:
- -
- Synonyms:
- Tiff66
- Chromosome:
- 6q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-13
- Date modifiied:
- 2016-10-05
Related products to: VNN1 antibody
Related articles to: VNN1 antibody
- Excessive neutrophil extracellular traps (NETs) formation worsens disease progression in sepsis. Vascular non-inflammatory molecule 1 (VNN1) is a glycosylphosphatidylinositol-anchored protein. The present study investigated the mechanism of the role of VNN1 in NETs formation and sepsis. - Source: PubMed
Publication date: 2026/07/15
Meng ShishuaiMa XinyueYang WeiZhao Mingyan - Early-life exposure to fine particulate matter (PM₂.₅) is increasingly implicated in the developmental origins of chronic respiratory diseases; however, the underlying molecular mechanisms remain poorly defined. This study employed Weighted Gene Co-expression Network Analysis (WGCNA) to investigate transcriptomic alterations associated with intrauterine and early neonatal PM₂.₅ exposure in the developing murine lung. Microarray data (GSE104656) spanning embryonic (E14.5, E18.5) and postnatal (P40) stages were processed using robust normalization and variance filtering to construct a scale-free co-expression network. Principal component analysis revealed that developmental maturation was the primary driver of global transcriptional variation, with no distinct separation attributable to PM₂.₅ exposure. WGCNA identified biologically relevant gene modules involved in immune and metabolic processes as well as cell cycle regulation, that exhibited strong correlations with developmental progression. Functional enrichment analysis confirmed significant involvement in immune activation, leukocyte adhesion, DNA replication, and chromosomal organisation. Although differential expression analysis under stringent thresholds did not detect significant PM₂.₅-responsive genes, integrative network analysis identified eleven exposure-associated genes embedded within key modules. These genes, including Vnn1, Gprc6a, Mfap1a, Rgs16, and Fpr1, represent highly connected hub nodes implicated in oxidative stress regulation, extracellular matrix remodelling, metabolic signalling, and immune modulation. It was concluded that early-life PM₂.₅ exposure did not globally disrupt lung transcriptomic architecture but selectively perturbs critical hub genes within developmental networks. This targeted sub-network vulnerability provided a mechanistic basis for the developmental programming of COPD susceptibility, linking early environmental insults to long-term respiratory dysfunction. - Source: PubMed
Publication date: 2026/07/04
Shittu S AAlimi A SShittu S T - Vanin-1 (VNN1) is crucial in inflammatory response and oxidative stress (OS), yet its contribution to sepsis remains unidentified. In this study, we investigated the functions of VNN1 in sepsis. Our results indicated VNN1 was elevated in sepsis patients and positively correlated with various cytokines. Meanwhile, VNN1 elevated in a mouse model of sepsis. In VNN1 knockout (KO) mice, VNN1 deficiency improved survival and organ function following CLP-induced sepsis. Furthermore, sepsis-induced inflammation and OS were reduced in VNN1 KO mice. Furthermore, our findings indicated VNN1 deficiency alleviated sepsis by regulating NF-kB/PPARγ pathways. Finally, the results showed VNN1 increased in sepsis patients, and higher VNN1 were associated with a poorer prognosis of sepsis. Our findings revealed a novel molecular mechanism in which VNN1 participated in sepsis by regulating NF-kB/PPARγ. This study offered a new strategy for inhibiting sepsis by targeting VNN1 signaling pathways. - Source: PubMed
Publication date: 2026/06/28
Wang Cheng-ChengMa Xin-XinZhu Chang-BaoZhang FeiXu GangShi Qing-HaiLu Hong-XiangZhang An-Qiang - Delayed fracture healing is a significant clinical challenge. Patients with concurrent traumatic brain injury (TBI) exhibit accelerated fracture healing; however, the underlying mechanisms remain poorly understood. This study aimed to identify key genes and molecular pathways that mediate enhanced fracture healing in patients with TBI. - Source: PubMed
Publication date: 2026/06/26
Wang BinLi ShentaiTong JiuhuiZhang HuaMa Wei - Acute respiratory distress syndrome (ARDS) is associated with high mortality, and increasing evidence suggests that air pollution may contribute to its development. However, the molecular mechanisms linking pollutant exposure to severe inflammatory lung injury remain incompletely understood. In this study, we integrated local clinical association data, bioinformatic analyses, molecular interaction prediction, and in vivo toxicological validation to investigate potential mechanisms underlying pollution-associated respiratory injury. Monthly hospital admissions for ARDS were positively associated with ambient particulate matter concentrations (PM and PM) in Yangzhou, China. Analysis of the GSE76293 dataset identified 167 overlapping genes between pollutant-related targets and ARDS-associated differentially expressed genes, which were mainly enriched in inflammatory and immune-response pathways. Machine learning prioritized three candidate targets, NLRC4, ETS2, and VNN1. Because polycyclic aromatic hydrocarbons (PAHs) are representative toxic components of particulate matter, benzo[a]pyrene (BaP) was selected for in vivo validation. Molecular docking and molecular dynamics analyses supported stable interactions between PAH-related compounds and the candidate proteins. In mice, BaP exposure induced acute lung injury, as indicated by histopathological damage, increased lung wet-to-dry weight ratio, and elevated inflammatory mediators in bronchoalveolar lavage fluid. BaP exposure was also accompanied by increased expression of NLRC4/GSDMD-related signaling, together with upregulation of ETS2 and VNN1 in lung tissue. These findings support a potential mechanistic link between particulate pollution-related toxicants and acute inflammatory lung injury relevant to ARDS. - Source: PubMed
Publication date: 2026/06/17
Song LinHe AifengJiang WeiLiu KeWang JingShi KeranYu JiangquanZheng Ruiqiang