Ask about this productRelated genes to: VTI1B antibody
- Gene:
- VTI1B NIH gene
- Name:
- vesicle transport through interaction with t-SNAREs 1B
- Previous symbol:
- -
- Synonyms:
- VTI2
- Chromosome:
- 14q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-22
- Date modifiied:
- 2016-10-05
Related products to: VTI1B antibody
Related articles to: VTI1B antibody
- Investigation of in utero, tissue-specific molecular pathways contributing to prenatal programming of childhood-onset asthma is needed to develop effective, targeted prevention strategies. We aimed to examine the relationship between predicted gene expression in placenta and childhood-onset asthma and to compare relationships between childhood- and adult-onset asthma. Asthma genome-wide association study published summary statistics were obtained from the UK Biobank and published placental gene expression quantitative trait loci were obtained from the Rhode Island Child Health Study. We used S-PrediXcan to evaluate and compare associations between placental predicted gene expression and childhood- and adult-onset asthma and to determine whether signals were placenta-specific. Among 8,038 tested placental predicted expression-asthma associations, we identified 56 (0.7%) genes only significantly associated with childhood-onset asthma, 12 (0.1%) genes only significantly associated with adult-onset asthma, and 18 (0.2%) shared genes. Predicted expression of several genes (ACTL9, AMN, C9orf38, C11orf30, CTSE, EFCAB13, EIF4E1B, FN1, GLS2, IL6, IVL, LZIC, MAN2A2, MEGT1, RACGAP1, SMAD6, SPATA5, TMEM25, VTI1B, WDR19) was not significantly associated with childhood- or adult-onset asthma in any non-placental tissue, suggesting that the associations may be placenta-specific. This study identified alterations in predicted expression of placental genes associated with transcriptional pathways critical to the development of asthma. We identified unique and shared pathways, particularly related to immune regulation, associated with childhood- and adult-onset. This expands our understanding of the fetal origins of asthma, highlights the placenta as an informative tissue in understanding asthma pathogenesis, and identifies target genes to prioritize for future functional studies. - Source: PubMed
Publication date: 2026/05/13
Jasper Elizabeth AMcKennan Christopher GThompson Emma ESchoettler NathanGebretsadik TebebHellwege Jacklyn NEdwards Todd LOber CaroleVelez Edwards Digna RHartert Tina VSnyder Brittney M - Malaria, caused by parasites, remains a global health crisis, necessitating novel therapeutic strategies targeting host-parasite interactions. During liver-stage infection, parasites exploit host vesicular trafficking machinery, particularly SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) proteins that mediate membrane fusion. Using a CRISPR/Cas9 knockout system in HeLa cells combined with advanced microscopy of -infected HeLa cells, we identified specific endolysosomal SNAREs including Vesicle-Associated Membrane Protein 7 (VAMP7), Vesicle-Associated Membrane Protein 8 (VAMP8), Vesicle Transport Through Interaction With T-SNAREs 1B (Vti1B), and Syntaxin 7 (Stx7) to be recruited to the parasitophorous vacuole membrane (PVM) with distinct temporal profiles. This demonstrates the parasite's precise manipulation of host endolysosomal trafficking pathways. VAMP7 and Vti1B were localized to the PVM within 30 min post-infection, suggesting potential roles during invasion, while VAMP8 and Stx7 appeared later around 24 h post infection (hpi), coinciding with increased nutrient acquisition. Single gene deletions showed minimal impact, but combinatorial knockouts (KO) revealed critical redundancy. VAMP7-VAMP8 as well as VAMP7-Vti1B double KO significantly reduced parasite infection and growth, with Vti1B playing a dominant role. Triple KO phenotypes mirrored VAMP7-Vti1B disruption, underscoring Vti1B's dominant role. SNARE depletion also impaired the lysosome-PVM association and LAMP1 positive vesicle recruitment. Our findings indicate hijacks a coordinated host SNARE network to fuse lysosomes with the PVM for nutrient uptake. Targeting Vti1B-containing complexes disrupts this pathway without host cell toxicity, offering a promising host-directed antimalarial approach. - Source: PubMed
Publication date: 2026/03/25
Atchou KodzoKramer NicolasBindschedler AnninaSchmuckli-Maurer JacquelineCaldelari RetoHeussler Volker T - 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 - Secretory granules (SGs) in endocrine cells store and release peptide hormones with their turnover tightly controlled to maintain cellular hormone levels. We found that crinophagy, a specialized autophagy process, is the prevalent pathway that degrades older unused SGs in resting cells by SG-lysosome fusion. siRNA screening with a live cell assay for SG-lysosome merge identified SG components Rab27A, Munc13-4 and VAMP2 and lysosomal components PLEKHM1, HOPS subunits, and SNAREs STX7, STX8, and VTI1B required for docking SGs to and fusion with lysosomes. Munc13-4 is a central regulator of crinophagy that associates with many proteins that are functionally essential for the merge of SGs with lysosomes, and regulates the docking and fusion of SGs with lysosomes. SG-lysosome fusion was regulated by local or global calcium through binding and activation of Munc13-4. The findings reveal the critical docking/fusion machinery for mediating SG turnover in mammalian endocrine cells, and indicate how its dysregulation could impair hormonal and metabolic regulation. - Source: PubMed
Publication date: 2025/09/04
Mani MuralidharanJames Declan JMartin Thomas F J