ArticleMolecular and cellular biology2003
Deletion of the SNARE vti1b in mice results in the loss of a single SNARE partner, syntaxin 8.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 119 citations in OpenAlex.
- Multiple overlapping SNARE complexes drive endosome maturation in Drosophila nephrocytes.Nature communications · 2026Article
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- Alterations in bone malformation in the absence of the endosomal SNAREs Vti1a and Vti1b.PloS one · 2026Article
- Autophagy Modulation by Antidepressants: Mechanisms and Implications.Neurochemical research · 2025Review
- Pharmacological mechanism of natural products to treat osteoporosis: a focus on the autophagy.Frontiers in pharmacology · 2025Review
- Monocytic Differentiation of Human Acute Myeloid Leukemia Cells: A Proteomic and Phosphoproteomic Comparison of FAB-M4/M5 Patients with and without Nucleophosmin 1 Mutations.International journal of molecular sciences · 2024Article
- Review
- Primary neurons lacking the SNAREs vti1a and vti1b show altered neuronal development.Neural development · 2022Article
- Targeting autophagy regulation in NLRP3 inflammasome-mediated lung inflammation in COVID-19.Clinical immunology (Orlando, Fla.) · 2022Review
- Vesicle trafficking and vesicle fusion: mechanisms, biological functions, and their implications for potential disease therapy.Molecular biomedicine · 2022Review
- Structural variants and tandem repeats in the founder individuals of four FBMC genomics · 2022Article
- Research Progress and Prospects of Autophagy in the Mechanism of Multidrug Resistance in Tumors.Journal of oncology · 2022Review
- The SNARE protein Vti1b is recruited to the sites of BCR activation but is redundant for antigen internalisation, processing and presentation.Frontiers in cell and developmental biology · 2022Article
- The Role of Vti1a in Biological Functions and Its Possible Role in Nervous System Disorders.Frontiers in molecular neuroscience · 2022Review
- Neuroinflammation in neurological disorders: pharmacotherapeutic targets from bench to bedside.Metabolic brain disease · 2021Review
- Review
- Synergies in exosomes and autophagy pathways for cellular homeostasis and metastasis of tumor cells.Cell & bioscience · 2020Review
- Distinct role of autophagy on angiogenesis: highlights on the effect of autophagy in endothelial lineage and progenitor cells.Stem cell research & therapy · 2018Review
- Vti1a/b regulate synaptic vesicle and dense core vesicle secretion via protein sorting at the Golgi.Nature communications · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SNARE proteins participate in recognition and fusion of membranes. A SNARE complex consisting of vti1b, syntaxin 8, syntaxin 7, and endobrevin/VAMP-8 which is required for fusion of late endosomes in vitro has been identified recently. Here, we generated mice deficient in vti1b to study the function of this protein in vivo. vti1b-deficient mice had reduced amounts of syntaxin 8 due to degradation of the syntaxin 8 protein, while the amounts of syntaxin 7 and endobrevin did not change. These data indicate that vti1b is specifically required for the stability of a single SNARE partner. vti1b-deficient mice were viable and fertile. Most vti1b-deficient mice were indistinguishable from wild-type mice and did not display defects in transport to the lysosome. However, 20% of the vti1b-deficient mice were smaller. Lysosomal degradation of an endocytosed protein was slightly delayed in hepatocytes derived from these mice. Multivesicular bodies and autophagic vacuoles accumulated in hepatocytes of some smaller vti1b-deficient mice. This suggests that other SNAREs can compensate for the reduction in syntaxin 8 and for the loss of vti1b in most mice even though vti1b shows only 30% amino acid identity with its closest relative.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.