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
- Chronic recurrent multifocal osteomyelitis (CRMO) is a pediatric autoinflammatory bone disease with poorly defined pathophysiology and limited biomarkers. Murine models implicate neutrophils, neutrophil-derived IL-1β, and the adaptor protein PSTPIP2, but direct evidence in human CRMO is lacking. This study aims to translate findings from mouse models to human disease by investigating the role of neutrophils and PSTPIP2 in CRMO. - Source: PubMed
Publication date: 2026/09/29
Pavliuchenko NataliiaDaněk PetrMalcová HanaHorváth RudolfCebecauerová DitaBrdička Tomáš - Myocardial ischemia/reperfusion (I/R) injury is a critical factor contributing to adverse outcomes following infarction, primarily due to oxidative stress, inflammation, and cardiomyocyte death. Vanin-1 (VNN1), a pantetheinase enzyme involved in redox regulation, has recently emerged as a potential mediator of tissue damage under stress conditions. This study aimed to investigate the role of VNN1 in hypoxia/reoxygenation (H/R)-induced injury in H9c2 cardiomyocytes and to explore the involvement of the PI3K/Akt axis. An H/R model was established using H9c2 cells, and VNN1 knockdown was achieved shRNA. Cellular injury, inflammation, and oxidative stress were assessed using viability assays, LDH release, ELISA, ROS detection, and biochemical analysis. Results revealed that VNN1 expression was significantly upregulated in H/R-treated cells. Silencing VNN1 mitigated cell damage, reduced pro-inflammatory cytokine release, and alleviated oxidative stress. Mechanistically, these protective effects were dependent on activation of the PI3K/Akt signaling axis, as inhibition of this pathway reversed the benefits of VNN1 knockdown. In conclusion, VNN1 knockdown confers protection against H/R-induced cardiomyocyte injury activating the PI3K/Akt pathway, highlighting VNN1 as a potential target for myocardial I/R injury. - Source: PubMed
Publication date: 2026/09/16
Hu XujiaoFang Yu - This study investigates the molecular and biophysical changes in Tumor-Associated Macrophage (TAM)-derived exosomes (TAME) compared to exosomes from non-tumor microenvironment (TE) macrophages (MO-E). TAMs are immune cells infiltrating tumors that promote cancer progression. - Source: PubMed
Publication date: 2026/05/12
Kulkarni T KBanerjee ABanerjee NCuffee JNewell SArmstrong EDeloatch S NPark J JongEl-Hashash A HBhattacharya SBanerjee H - Equine asthma (EA) is the most prevalent chronic respiratory disease in horses, but molecules thought to be relevant in its pathogenesis are not yet fully understood. Recently, increased Vanin-1 (VNN1) levels were found in bronchoalveolar lavage fluid from horses with severe EA. Human VNN1 is known as a pantetheinase, which is associated with respiratory diseases such as asthma, but the equine vanins (eVNNs) are uncharacterized. We identified the domain architecture of eVNN in silico and analyzed its tissue expression in healthy horses using RT-PCR (=5) and in situ hybridization (=3). Recombinant eVNNs were expressed in HEK293 cells to assess cellular transport and glycosylation via Endo H and PNGase F treatment. Three putative functional were identified on chromosome 10, each containing canonical Nitrilase superfamily domains. All genes showed a broad tissue expression, but distinct airway localization: and were predominantly expressed in respiratory epithelium, whereas was localized in submucosal glands. eVNN1 and eVNN3 were secreted, while eVNN2 remained cell associated. Pantetheinase activity of recombinant eVNN1 was confirmed by mass spectrometry. The three eVNNs appear to cover different functional niches in equine airways, enabling future research into their putative role in EA. - Source: PubMed
Publication date: 2026/08/31
Landmann KatharinaBartenschlager FlorianMeierhofer DavidSpree AndreasPisch CarolineZeyner AnnetteSchnabel Christiane LMundhenk Lars - 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