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
- Persistent symptoms following SARS-CoV-2 infection are the hallmark of post-COVID condition (PCC), also referred to as long COVID. However, the underlying molecular mechanisms remain poorly understood. In this study, we employed data-independent acquisition mass spectrometry (DIA-MS)-based plasma proteomics to identify molecular alterations associated with PCC. DIA-MS proteomic analysis revealed a clear distinction between the plasma proteome of uninfected individuals and those previously infected with SARS-CoV-2, irrespective of PCC status. PCC samples demonstrated downregulation of the antioxidant protein peroxiredoxin 6 (PRDX6) and upregulation of oxidative stress-associated proteins, particularly vanin-1 (VNN1) and paraoxonase-3 (PON3). Additionally, individuals with PCC exhibited significantly elevated levels of six proteins-PCSK9, CST3, C1Q, CPB2, KNG1, and GAPDH-associated with glycolysis, complement and coagulation cascades, and inflammatory pathways. Validation by ELISA does not necessarily reflect the proteomics data suggesting the requirement for alternate methods of validation. Nonetheless, oxidative stress, as measured by 8-hydroxy-2'-deoxyguanosine (8-OHdG), further showed that PCC samples had significantly higher levels of DNA damage, compared with convalescent individuals. Antioxidant markers, including reduced and oxidized glutathione (GSH and GSSG), were significantly lower in PCC samples than in uninfected controls. Collectively, these findings indicate that plasma proteomic alterations persist for at least 3 months following SARS-CoV-2 infection, with additional disruptions in oxidative stress and inflammatory pathways characterizing individuals with PCC. - Source: PubMed
Publication date: 2026/04/17
Chowdhury Mohammad Mobarak HQuenum Akouavi Julite IrmineRioux-Perreault ChristineLucier Jean-FrançoisIlangumaran SubburajPiché AlainAllard-Chamard HuguesRamanathan Sheela - Acute myocardial infarction (AMI) ranks among the leading causes of death globally and is linked to obesity and the metabolism of lipids. The objective of this research was to develop an innovative predictive model utilizing obesity and lipid metabolism-related genes (OLMRGs) to facilitate the diagnosis and molecular typing of AMI. - Source: PubMed
Publication date: 2026/03/27
Li JianhuaXue ZixinZhang MinLu FengJi Shaoping - Acute kidney injury (AKI) is a short-term clinical condition that results in a decline in renal function. The pathophysiology of AKI was influenced by a variety of pathways, one of which is oxidative stress (OS). The development of AKI was aided by increased OS from reactive oxygen species (ROS) and inadequate antioxidant mechanisms. Effective early biomarkers and treatment approaches for AKI are still lacking; however, the widespread use of bioinformatic analysis may help. - Source: PubMed
Du YiweiLi Yinghao - This experiment was conducted to explore the effects of betaine on the DNA methylation level, expression level, and fat synthesis of in goose hepatocytes by isolating the primary hepatocytes of goose at the cellular level and constructing a fatty degeneration model of goose hepatocytes. In the study, 23-day-old Taizhou goose embryos were used as the research object, and free fatty acid (PA:OA = 2:1) was used to induce steatosis of goose primary hepatocytes. The experiment was randomly divided into seven groups: control group, steatosis model group, and betaine (2, 10, 25, 50, 100mM) group. After 24 h of cell culture, cell viability, oil red O staining, and lipid metabolism-related indicators in cell supernatant were measured, and cells were collected to determine , , , , gene expression and promoter region DNA methylation level. (1) The addition of 0.5 mM fatty acids successfully determined the degeneration of goose hepatocytes. The levels of TG and LDL were significantly increased ( < 0.05), and the level of HDL was significantly decreased. (2) The addition of 100 mM betaine significantly reduced TG levels, and 10, 25, 50, and 100 mM betaine significantly reduced LDL levels. The addition of betaine had no significant effect on HDL level compared to the FFA group ( > 0.05), although a significant overall model effect was observed. Oil red O staining showed that the area of lipid droplets in cells with 50 mM betaine decreased most significantly. (3) The expression levels of , , , , and genes in the fat model group were significantly higher compared to the control group ( < 0.05), and the DNA methylation level in the promoter region of the gene decreased. (4) The addition of 2, 10, 25, 50, and 100 mM betaine significantly reduced the expression of . The expression of in 2, 10, and 25 mM betaine groups significantly decreased. Betaine at 10 and 100 mM significantly reduced the expression of , but it showed no significant effect on expression. Addition of 2, 50, and 100 mM betaine led to an increased DNA methylation status at the gene promoter region. In summary, the addition of betaine can reduce the expression of fatty acid synthesizing genes such as , , and , down-regulate the expression level of the gene, increase the DNA methylation level of the VNN1 promoter region, and reduce lipid deposition in goose liver steatosis cells. - Source: PubMed
Publication date: 2026/02/12
Yang ZhiNazir UsmanWang XinfangZheng XuchengYang HaimingWang Zhiyue - Circadian rhythms and depressive disorder (DD) are closely connected. Disrupted circadian rhythms can lead to or exacerbate symptoms of depression. From a transcriptomic perspective, this study aimed to explore the diagnostic potential of circadian rhythm-related genes (CRGs) as biomarkers for DD. Total RNA was extracted from whole-blood samples from 15 adolescent patients with DD and 15 age-matched controls collected under fasting conditions in the morning. Following RNA sequencing and quality control, a post hoc power analysis was performed to assess sample adequacy. The differential expression analysis revealed differentially expressed genes (DEGs) that intersected with a circadian rhythm-related gene set. A PPI network was constructed to identify hub genes. Diagnostic performance was evaluated in the training set using ROC curves and tenfold cross-validation and then validated in two independent datasets (GSE76826 and GSE32280). Biomarkers with a consistent AUC > 0.7 and expression trends were incorporated into a nomogram, which was assessed using calibration curves, the Hosmer-Lemeshow test, and decision curve analysis. GSEA, CIBERSORT immune cell infiltration analysis, and a predicted lncRNA-miRNA-mRNA network were used to explore the functions and mechanisms of the biomarkers. RT-qPCR was performed to validate gene expression in an independent cohort. CCL23 and VNN1 were identified as key circadian rhythm-related DD biomarkers and were consistently upregulated in samples from multiple datasets. They showed high diagnostic accuracy in the discovery cohort (AUC: 0.916 for CCL23 and 0.987 for VNN1) and maintained an AUC > 0.7 in the two independent validation cohorts. A nomogram integrating both biomarkers exhibited excellent predictive performance and clinical utility. Enrichment analysis revealed that DEGs were associated with pathways including "cardiac muscle contraction", "ribosome" and "neuroactive ligand-receptor interaction". CCL23 was linked to the "proteasome" and "long-term potentiation", and VNN1 was linked to the "spliceosome" and "oxidative phosphorylation". Both biomarkers were coenriched in "benzodiazepine receptor activity", implicating the GABAergic system. Immune profiling revealed altered infiltration of 10 immune cell types in DD patients, with a positive correlation between the expression of CCL23 and the number of naive B cells (r = 0.5; P = 0.0046). Single-cell RNA sequencing indicated low but detectable expression across major neuronal and glial cell types. A predicted ceRNA network suggested that regulators such as AC000120.1 and AC079781.5 may target VNN1 via miRNAs (e.g., hsa-miR-1185-5p). RT‒qPCR confirmed the significant upregulation of the expression of both biomarkers in DD patients compared with controls (P < 0.05). Two CRGs (CCL23 and VNN1) were identified as biomarkers for DD and exhibited excellent diagnostic performance. These findings provide promising prospects for future DD research. - Source: PubMed
Publication date: 2026/02/18
Liang JiaLu CaifangChen LipingFan YanhuaHuang FengyanWei WenjiaKang HongHuang SixieLu HaiqingPan MiaoShen BingXu Ai