ArticleMolecular biology of the cell2011
Vacuolar H(+)-ATPase subunits Voa1 and Voa2 cooperatively regulate secretory vesicle acidification, transmitter uptake, and storage.
Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Deep Proteome Profiling of Rat Dorsal Striatal Synaptoneurosomes Following Methamphetamine Exposure.ACS chemical neuroscience · 2026Article
- The a subunit isoforms of V-ATPase are involved in glucose-dependent trafficking of insulin granules.Scientific reports · 2025Article
- The Emerging Roles of Vacuolar-Type ATPase-Dependent Lysosomal Acidification in Cardiovascular Disease.Biomolecules · 2025Review
- Tcirg1 deficiency delays osteoarthritis progression by impairing lysosome acidification and peripheral accumulation in osteoclasts.Frontiers in cell and developmental biology · 2025Article
- Loss of the Golgi-localized v-ATPase subunit does not alter insulin granule formation or pancreatic islet β-cell function.American journal of physiology. Endocrinology and metabolism · 2024Article
- Structural and functional understanding of disease-associated mutations in V-ATPase subunit a1 and other isoforms.Frontiers in molecular neuroscience · 2023Review
- Protein mishandling and impaired lysosomal proteolysis generated through calcium dysregulation in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- NGF-Induced Upregulation of CGRP in Orofacial Pain Induced by Tooth Movement Is Dependent on Atp6v0a1 and Vesicle Release.International journal of molecular sciences · 2022Article
- Astrocytic Glutamatergic Transmission and Its Implications in Neurodegenerative Disorders.Cells · 2022Review
- Detection and quantification of the vacuolar H+ATPase using the Legionella effector protein SidK.The Journal of cell biology · 2022Article
- The V-ATPaseInternational journal of molecular sciences · 2021Review
- Regulation and function of V-ATPases in physiology and disease.Biochimica et biophysica acta. Biomembranes · 2020Review
- Sugary Logistics Gone Wrong: Membrane Trafficking and Congenital Disorders of Glycosylation.International journal of molecular sciences · 2020Review
- Investigation of Isoform Specific Functions of the V-ATPase a Subunit DuringFrontiers in genetics · 2020Article
- The priming factor CAPS1 regulates dense-core vesicle acidification by interacting with rabconnectin3β/WDR7 in neuroendocrine cells.The Journal of biological chemistry · 2019Article
- Article
- Human Macrophages Clear the Biovar Microtus Strain ofFrontiers in cellular and infection microbiology · 2019Article
- Observations From a Mouse Model of Forebrain Voa1 Knockout: Focus on Hippocampal Structure and Function.Frontiers in cellular neuroscience · 2019Article
- HID-1 controls formation of large dense core vesicles by influencing cargo sorting andMolecular biology of the cell · 2017Article
- F-actin reorganization by V-ATPase inhibition in prostate cancer.Biology open · 2017Article
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Authors and funding
11 authors.
Funding
Abstract
The Vo sector of the vacuolar H(+)-ATPase is a multisubunit complex that forms a proteolipid pore. Among the four isoforms (a1-a4) of subunit Voa, the isoform(s) critical for secretory vesicle acidification have yet to be identified. An independent function of Voa1 in exocytosis has been suggested. Here we investigate the function of Voa isoforms in secretory vesicle acidification and exocytosis by using neurosecretory PC12 cells. Fluorescence-tagged and endogenous Voa1 are primarily localized on secretory vesicles, whereas fluorescence-tagged Voa2 and Voa3 are enriched on the Golgi and early endosomes, respectively. To elucidate the functional roles of Voa1 and Voa2, we engineered PC12 cells in which Voa1, Voa2, or both are stably down-regulated. Our results reveal significant reductions in the acidification and transmitter uptake/storage of dense-core vesicles by knockdown of Voa1 and more dramatically of Voa1/Voa2 but not of Voa2. Overexpressing knockdown-resistant Voa1 suppresses the acidification defect caused by the Voa1/Voa2 knockdown. Unexpectedly, Ca(2+)-dependent peptide secretion is largely unaffected in Voa1 or Voa1/Voa2 knockdown cells. Our data demonstrate that Voa1 and Voa2 cooperatively regulate the acidification and transmitter uptake/storage of dense-core vesicles, whereas they might not be as critical for exocytosis as recently proposed.
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