Ask about this productRelated genes to: VTI1A antibody
- Gene:
- VTI1A NIH gene
- Name:
- vesicle transport through interaction with t-SNAREs 1A
- Previous symbol:
- -
- Synonyms:
- MVti1, Vti1a, Vti1-rp2
- Chromosome:
- 10q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-22
- Date modifiied:
- 2014-11-18
Related products to: VTI1A antibody
Related articles to: VTI1A antibody
- Absence of the endosomal SNAREs vti1a and vti1b results in perinatal death and severe neuronal phenotypes in mice, while lack of one of these proteins results in minor phenotypes. Proteomic differences were investigated to obtain a deeper insight into processes in which vti1a and vti1b are involved. Here we applied a bottom-up shotgun proteomic approach to investigate the differences in wild-type, double heterozygous (DHET), vti1a vti1b double knockout (DKO), vti1a knockout and vti1b knockout cerebral cortices. Single deletions did not affect protein levels significantly. A total of 1725 proteins were detected of which 69 were less abundant and 191 proteins were more abundant in DKO cortices. Many less abundant proteins belonged to cellular components and reactome pathways synapse, synaptic vesicle cycle, vesicle mediated transport, L1CAM interaction, and cholesterol biosynthesis in pathway enrichment analysis. More abundant proteins were enriched in cellular components and Kyoto Encyclopaedia of Genes and Genomes (KEGG)-pathways such as spliceosome, ribosome, carbon metabolism, and ribonucleoprotein complex. Immunoblotting validated reduced expression levels of the tested synaptic vesicle proteins as well as increased amounts of lysophosphatidylcholine acyltransferase 1 (Lpcat1) and neuron-specific gene 2 (Nsg2), which is involved in postsynaptic AMPA-receptor recycling. These data indicate that the synapse and cell adhesion were strongly affected in DKO brains. STATEMENT OF SIGNIFICANCE OF THE STUDY: Distinct populations of neurons and glia cells are generated and organize into layers during brain development. Neurons develop an elaborate morphology to transmit information via axons and synapses to dendrites in receiving neurons. These neurites form via several specialized pathways of vesicle secretion and endocytosis. Fusion between these membranes requires members of the SNARE protein family. Double knockouts of the endosomal SNAREs vti1a and vti1b (DKO) result in perinatal lethality in mice with massive defects in the brain. In this study we compared the proteome of DKO brain cortices with double heterozygous controls to obtain insights into the molecular alterations and affected pathways. DKO brains contained lower amounts of synaptic proteins and proteins involved in cell adhesion, membrane trafficking and cholesterol biosynthesis. Several proteins of spliceosomes, ribosomes and carbon metabolism were more abundant in DKO brains, which may be a consequence of the reduced amounts of synaptic proteins or a shift in cell populations. Lysophosphatidylcholine acyltransferase 1 (Lpcat1) and neuron-specific gene 2 (Nsg2), which is involved in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) recycling, were confirmed to be more abundant by Western blotting. These data point to defects in trafficking especially in the synapse and in cell adhesion, which is required for neurite outgrowth. - Source: PubMed
Publication date: 2026/03/20
Gottschalk JuliaKotschnew KatharinaHahn JuliaPatschkowski Thomasvon Fischer von Mollard Gabriele - The Qb-SNAREs (soluble N-ethylmaleimide-sensitive-factor attachment receptor) Vti1a and Vti1b participate in membrane fusion in the endosomal system of mammalian cells and are partially redundant. While double deficiency of Vti1a-/-Vti1b-/- (DKO) is perinatal lethal, double heterozygous Vti1a+/-Vti1b+/- (DHET) mice presented no phenotypic alterations when compared to wild-type mice. To investigate the physiological role of these proteins, this study focused on the analysis of embryonic DKO versus DHET mice. The size and weight of E18.5 DKO embryos were significantly lower when compared with those of DHET littermates and wild-type embryos. Furthermore, we observed alterations in skeletal development of DKO embryos, mainly in the front limbs, ribs, clavicles and sternum. A lumbar vertebra was missing in DKO embryos and the palate was not closed in 50% of these embryos. - Source: PubMed
Publication date: 2026/03/16
Schmücker SimoneSchöning SusanneWiegand ChristianeHöfling Sascha MichaelBollmann ChristianKoliwer JudithFischer von Mollard Gabriele - Epigenetic alterations, particularly DNA methylation, play a crucial role in the progression of oral squamous cell carcinoma (OSCC) from oral leukoplakia (OL). However, the molecular mechanisms driving this transition remain poorly understood. Using interpretable machine learning (IML) on genome-wide methylation data from 118 samples (22 OL, 74 OSCC, and 22 controls), we identified 20 key CpG sites among 820 193 loci through SHAP (SHapley Additive exPlanations) analysis. Notably, cg19853638, cg25393842, cg01743793, and cg10784570 mapped to pivotal genes such as TNFRSF19, ALOX5, and SH3PXD2A, which regulate cell morphology, inflammatory pathways, and immune responses- critical processes influencing OSCC malignancy and progression. To assess generalizability and confirm the robustness of classifier, the predictive model was validated on an independent Taiwanese cohort (GSE38532) profiled on a different array platform, achieving 98.8% accuracy and ROC-AUC of 0.999 demonstrating robust cross-population performance. Furthermore, cross-omics integration with an independent transcriptomic dataset (GSE31056) identified eight genes, including ALOX5, FOXP1, and VTI1A, showing consistent methylation and expression patterns, underscoring their biological relevance. Our findings highlight the functional relevance of SH3PXD2A, TNFRSF19, and ALOX5 in OSCC pathophysiology: SH3PXD2A mediates cell migration and invasion, TNFRSF19 is involved in survival signaling, and ALOX5 regulates inflammatory responses. These multi-layered analyses provide novel insights into epigenetic mechanisms underlying OL to OSCC progression and highlight candidate biomarkers with strong translational potential. By combining IML based methylation modeling with external and cross-omics validation, this study advances the development of reliable, interpretable biomarkers for precision oral cancer diagnostics and management. - Source: PubMed
Yadav KhushiHasija Yasha - Emerging viral infections can initiate a global pandemic with high mortality. Understanding the immunopathogenesis of these viruses is critical to developing effective strategies for managing/preventing such outbreaks. - Source: PubMed
Publication date: 2025/12/29
Bouzid AmalYusuf Ayesha MMousa MiraVenkatachalam ThenmozhiTay GuanUddin MaimunahAlkaabi NawalAyad Maha SaberAlsafar HabibaHamoudi Rifat - Microexons exhibit striking evolutionary conservation and are subject to precise, switch-like regulation in neurons, orchestrated by the splicing factors and . Disruption of these regulators in mice leads to severe neurological phenotypes, and their misregulation is linked to human disease. However, the specific microexons involved in these phenotypes and the effects of individual microexon deletions on neurodevelopment, physiology, and behavior remain poorly understood. To explore this, we generated zebrafish lines with deletions of 18 individual microexons, alongside and mutant lines, and conducted comprehensive phenotypic analyses. We discovered that while loss of , alone or together with , resulted in significant alterations in neuritogenesis, locomotion, and social behavior, individual microexon deletions typically produced mild or no noticeable effects. Nonetheless, we identified specific microexons associated with defects in neuritogenesis (, , , ) and social behavior (, ). Additionally, most microexon deletions triggered coordinated transcriptomic changes in neural pathways, suggesting the presence of molecular compensatory mechanisms. Our findings suggest that the severe phenotypes caused by depletion arise from the combined effects of multiple subtle disruptions across various cellular pathways, which are individually well-tolerated. - Source: PubMed
Publication date: 2025/11/18
Lopez-Blanch LauraRodríguez-Marin CristinaMantica FedericaIñiguez Luis PPermanyer JonKita Elizabeth MMackensen TahneeCodina-Tobias MireiaRomero-Ferrero FranciscoFernandez-Albert JordiCuadrado MyriamBustelo Xosé Rde Polavieja GonzaloIrimia Manuel