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Published on: June 16, 2023
The V-type H+-ATPase in vesicular trafficking: targeting, regulation and function
Vladimir Marshansky1, Masamitsu Futai
1Program in Membrane Biology, Center for Systems Biology, Simches Research Center, CPZN No. 8212, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA. Marshansky.Vladimir@mgh.harvard.edu
V-ATPase is a key enzyme that acidifies vesicles in eukaryotic cells. This acidification is essential for the proper functioning of both exocytotic and endocytotic pathways. Recent studies show that when V-ATPase is not working properly, it can lead to disruptions in trafficking and contribute to disease. This review summarizes the latest findings on how V-ATPase regulates these processes and its potential role in disease. The authors highlight the enzyme's direct influence on trafficking events and suggest it may be a target for future therapies.
Area of Science:
- Cell biology
- Membrane transport mechanisms
- V-ATPase regulation in vesicular trafficking
Background:
V-ATPase activity is known to regulate organellar pH. This process is critical for vesicle transport in eukaryotic cells. However, the precise mechanisms remain unclear. Recent studies suggest a link between V-ATPase dysfunction and disease. No prior work had fully explained these connections. Acidification defects appear in multiple disease contexts. This gap motivated the current review. The goal is to clarify V-ATPase's role in trafficking and disease.
Purpose Of The Study:
This review aims to clarify the role of V-ATPase in vesicular trafficking. It focuses on recent findings about regulation and function. The authors highlight how acidification affects transport. They address gaps in understanding disease mechanisms. The study emphasizes direct roles of V-ATPase in trafficking. It does not propose new hypotheses. Instead, it synthesizes current evidence. The goal is to inform future research directions.
Main Methods:
The authors conducted a literature-based review. They analyzed recent studies on V-ATPase function. They focused on exocytotic and endocytotic pathways. The review includes findings on acidification mechanisms. They examined how V-ATPase influences trafficking. The approach combines biochemical and cell biological data. They highlight studies on human disease models. The synthesis emphasizes direct regulatory roles.
Main Results:
V-ATPase activity is essential for vesicle acidification. This process supports trafficking in both pathways. Acidification defects disrupt normal transport. Recent studies show V-ATPase regulates membrane fusion. It also controls cargo sorting and vesicle formation. The enzyme influences pH-dependent signaling. These findings clarify disease mechanisms. They suggest V-ATPase as a potential therapeutic target.
Conclusions:
The review confirms V-ATPase's role in vesicular trafficking. It supports the enzyme's function in acidification. The data show how pH affects transport events. The authors propose V-ATPase as a disease-related target. They emphasize the need for further research. No prior work had resolved these connections. The review does not claim V-ATPase is the only factor. It highlights the importance of acidification in trafficking.
Frequently Asked Questions
V-ATPase drives proton pumping to acidify vesicles, which is essential for trafficking events.
Defective V-ATPase acidification is linked to multiple human diseases and is a potential therapeutic target.
Acidification helps in cargo sorting, membrane fusion, and signaling during vesicular trafficking.
Both exocytotic and endocytotic pathways depend on V-ATPase-driven acidification.
Recent studies show V-ATPase regulates membrane fusion and influences pH-dependent signaling.
The authors suggest V-ATPase may be a potential target for treating acidification-related diseases.
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