ArticleMolecular biology of the cell2018
ATP6AP2 functions as a V-ATPase assembly factor in the endoplasmic reticulum.
Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- A mycobacterial Sec61 inhibitor disrupts lysosome function by blocking Vacuolar-ATPase biosynthesis.European journal of cell biology · 2026Article
- The anion channel GPR89 is a tumor-specific dependency in breast cancer.Nature communications · 2026Article
- ATP6AP2 ameliorates inflammation and pyroptosis in heart failure by promoting lysosome-dependent STING degradation.Apoptosis : an international journal on programmed cell death · 2026Article
- Failure of lysosomal acidification and endomembrane network in neurodegeneration.Experimental & molecular medicine · 2025Review
- Recent advances in the clinical spectrum and pathomechanisms associated with X-linked myopathy with excessive autophagy and otherJournal of neuromuscular diseases · 2025Review
- Vacuolar HJournal of cellular physiology · 2025Article
- Comparative proteomics of HepG2 cells reveals NGLY1 as an important regulator of ferroptosis resistance and iron uptake.PloS one · 2025Article
- Review
- Dmxl1 Is an Essential Mammalian Gene that Is Required for V-ATPase Assembly and Function In Vivo.Function (Oxford, England) · 2024Article
- Targeting the High-Density Lipoprotein Proteome for the Treatment of Post-Acute Sequelae of SARS-CoV-2.International journal of molecular sciences · 2024Article
- Aberrant Expressions ofCurrent genomics · 2023Article
- Resistance to Chemotherapeutic 5-Fluorouracil Conferred by Modulation of Heterochromatic Integrity through Ino80 Function in Fission Yeast.International journal of molecular sciences · 2023Article
- Mapping the protein binding site of the (pro)renin receptor using in silico 3D structural analysis.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Mutations in V-ATPase in follicular lymphoma activate autophagic flux creating a targetable dependency.Autophagy · 2023Article
- Expanding the phenotype and metabolic basis of ATP6AP2-congenital disorder of glycosylation in a Chinese patient with a novel variant c.185G>A (p.Gly62Glu).Frontiers in genetics · 2023Article
- Reduced gene dosage is a common mechanism of neuropathologies caused by ATP6AP2 splicing mutations.Parkinsonism & related disorders · 2022Article
- Follicular lymphoma-associated mutations in the V-ATPase chaperone VMA21 activate autophagy creating a targetable dependency.Autophagy · 2022Article
- Inhibition of endoplasmic reticulum stress signaling rescues cytotoxicity of human apolipoprotein-L1 risk variants in Drosophila.Kidney international · 2022Article
- "Nomen not est omen": the (pro)renin receptor and receptor-mediated endocytosis in the proximal tubule-a new (pro)renin-independent role forATP6ap2.Pflugers Archiv : European journal of physiology · 2021Article
- Regulation and function of V-ATPases in physiology and disease.Biochimica et biophysica acta. Biomembranes · 2020Review
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
ATP6AP2 (also known as the [pro]renin receptor) is a type I transmembrane protein that can be cleaved into two fragments in the Golgi apparatus. While in Drosophila ATP6AP2 functions in the planar cell polarity (PCP) pathway, recent human genetic studies have suggested that ATP6AP2 could participate in the assembly of the V-ATPase in the endoplasmic reticulum (ER). Using a yeast model, we show here that the V-ATPase assembly factor Voa1 can functionally be replaced by Drosophila ATP6AP2. This rescue is even more efficient when coexpressing its binding partner ATP6AP1, indicating that these two proteins together fulfill Voa1 functions in higher organisms. Structure-function analyses in both yeast and Drosophila show that proteolytic cleavage is dispensable, while C-terminus-dependent ER retrieval is required for ATP6AP2 function. Accordingly, we demonstrate that both overexpression and lack of ATP6AP2 causes ER stress in Drosophila wing cells and that the induction of ER stress is sufficient to cause PCP phenotypes. In summary, our results suggest that full-length ATP6AP2 contributes to the assembly of the V-ATPase proton pore and that impairment of this function affects ER homeostasis and PCP signaling.
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