ArticleScientific reports2022
The lysosomal V-ATPase a3 subunit is involved in localization of Mon1-Ccz1, the GEF for Rab7, to secretory lysosomes in osteoclasts.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Beyond the membrane: Internalization and compartmentalization of insulin‑like growth factor 1 receptor signaling in cancer pathogenesis and treatment (Review).International journal of oncology · 2026Review
- The a subunit isoforms of V-ATPase are involved in glucose-dependent trafficking of insulin granules.Scientific reports · 2025Article
- The spectrum of lysosomal stress and damage responses: from mechanosensing to inflammation.EMBO reports · 2025Review
- The different roles of V-ATPase a subunits in phagocytosis/endocytosis and autophagy.Autophagy · 2024Article
- Collapse of late endosomal pH elicits a rapid Rab7 response via the V-ATPase and RILP.Journal of cell science · 2024Article
- Collapse of late endosomal pH elicits a rapid Rab7 response via V-ATPase and RILP.bioRxiv : the preprint server for biology · 2024Article
- The Human Mutation K237_V238del in a Putative Lipid Binding Motif within the V-ATPase a2 Isoform Suggests a Molecular Mechanism Underlying Cutis Laxa.International journal of molecular sciences · 2024Article
- Lysosomal biogenesis and function in osteoclasts: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- Structure and function of the membrane microdomains in osteoclasts.Bone research · 2023Review
- Rab32 and Rab38 maintain bone homeostasis by regulating intracellular traffic in osteoclasts.Cell structure and function · 2023Article
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Authors and funding
5 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
We have shown previously that the lysosomal a3 isoform of the a subunit of vacuolar-type ATPase (V-ATPase) interacts with inactive (GDP-bound form) Rab7, a small GTPase that regulates late endosome/lysosome trafficking, and that a3 recruits Rab7 to secretory lysosomes in mouse osteoclasts. This is essential for outward trafficking of secretory lysosomes and thus for bone resorption. However, the molecular mechanism underlying the recruitment of Rab7 by a3 remains to be fully elucidated. Here, we showed that a3 interacts with the Mon1A-Ccz1 complex, a guanine nucleotide exchange factor (GEF) for Rab7, using HEK293T cells. The interaction was mediated by the amino-terminal half domain of a3 and the longin motifs of Mon1A and Ccz1. Exogenous expression of the GEF promoted the interaction between a3 and Rab7. Mon1A mutants that interact inefficiently with Rab7 interacted with a3 at a similar level to wild-type Mon1A. Lysosomal localization of endogenous Ccz1 was abolished in osteoclasts lacking a3. These results suggest that the lysosomal a3 isoform of V-ATPase interacts with Mon1A-Ccz1, and that a3 is important for Mon1A-Ccz1 localization to secretory lysosomes, which mediates Rab7 recruitment to the organelle.
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