PIKfyve is required for efficient phagosomal Rab7 acquisition and the delivery and fusion of early macropinosomes to phagosomes.

A Drosophila model for Dent's disease type 1 revealed impaired endoplasmic reticulum export of Cubilin as pathogenic mechanism.

Mechanism of tcirg1b deficiency in disrupting central nervous system homeostasis of zebrafish.

V-ATPase a3 Directs Secretory Lysosome Transport in Enamel Formation.

ATP6V1C1 deficiency impairs auditory and vestibular hair cell function and leads to sensorineural hearing loss in humans and mice.

CELL DEATH1 safeguards microspore fate determination by repressing vacuole-executed programmed cell death.

Vacuolar-type H+-ATPase-mediated extra-organellar buffering resolves mitochondrial dysfunction.

A Reversible Mitochondrial ROS Probe for Monitoring Mitophagy Dynamics: Development and Application of MitoFlare.

Failure of lysosomal acidification and endomembrane network in neurodegeneration.

Effect of V-ATPase a3 subunit on microglial phagosome maturation in zebrafish.

Maturation stage-specific V-ATPase disassembly explains the neutral pH of mature mucocyst lysosome-related organelles in Tetrahymena thermophila.

ATP6AP2-Related Disease Caused by Splicing Defects: Abnormal Glycosylation and the First Affected Female.

The Christianson syndrome protein, sodium hydrogen exchanger isoform 6, is required for fat accumulation.

Modeling TCIRG1 Neutropenia by Utilizing Patient Derived Induced Pluripotent Stem Cells.

Bisphenol F disrupts lipophagy and lysosomal acidification via ATGL-SIRT1-PPARα signaling in NAFLD-like hepatic changes.

Control of Golgi- V-ATPase through Sac1-dependent co-regulation of PI(4)P and cholesterol.

Stress granule clearance mediated by V-ATPase-interacting protein NCOA7 mitigates ovarian aging.

Soma to neuron communication links stress adaptation to stress avoidance behavior.

Rag GTPases control lysosomal acidification by regulating v-ATPase assembly in Drosophila.

Oxr1 and Ncoa7 regulate V-ATPase to achieve optimal pH for glycosylation within the Golgi apparatus and trans-Golgi network.

Defective autophagy in a fibroin secretion-deficient silkworm mutant.

STING mediates lysosomal quality control and recovery through its proton channel function and TFEB activation in lysosomal storage disorders.

Atp6v0d2 deficiency partially restores defects in Mcoln1-deficient mouse corpus luteum.

V-ATPase contributes to the cariogenicity of Candida albicans- Streptococcus mutans biofilm.

Recent advances in the clinical spectrum and pathomechanisms associated with X-linked myopathy with excessive autophagy and other VMA21-related disorders.

Vacuolar (H+)-ATPase Genes Are Essential for Cuticle and Wing Development in Locusta migratoria.

Lysosomal quality control Review.

Golgi pH elevation due to loss of V-ATPase subunit V0a2 function correlates with tissue-specific glycosylation changes and globozoospermia.

Non-autophagic Golgi-LC3 lipidation facilitates TFE3 stress response against Golgi dysfunction.

V-ATPase Dysfunction in the Brain: Genetic Insights and Therapeutic Opportunities.

The V-ATPase complex component RNAseK is required for lysosomal hydrolase delivery and autophagosome degradation.

Dominantly acting variants in ATP6V1C1 and ATP6V1B2 cause a multisystem phenotypic spectrum by altering lysosomal and/or autophagosome function.

The V-ATPase/ATG16L1 axis is controlled by the V1H subunit.

On the coupling of intracellular K + ${{\rm{K}}}^{+}$ to glycolytic oscillations in yeast.

Deletion of VPS50 protein in mouse brain impairs synaptic function and behavior.

The different roles of V-ATPase a subunits in phagocytosis/endocytosis and autophagy.

HPS6 Deficiency Leads to Reduced Vacuolar-Type H+-ATPase and Impaired Biogenesis of Lamellar Bodies in Alveolar Type II Cells.

Lysosomal dysfunction and overload of nucleosides in thymidine phosphorylase deficiency of MNGIE.

Defective Lamtor5 Leads to Autoimmunity by Deregulating v-ATPase and Lysosomal Acidification.

Human V-ATPase function is positively and negatively regulated by TLDc proteins.

Epileptic encephalopathies and progressive neurodegeneration.

Impaired lysosomal acidity maintenance in acid lipase-deficient cells leads to defective autophagy.

Loss of the Golgi-localized v-ATPase subunit does not alter insulin granule formation or pancreatic islet β-cell function.

The Rogdi knockout mouse is a model for Kohlschütter-Tönz syndrome.

The hybrid RAVE complex plays V-ATPase-dependent and -independent pathobiological roles in Cryptococcus neoformans.

Rab32 and Rab38 maintain bone homeostasis by regulating intracellular traffic in osteoclasts.

Identification of a muscle-specific isoform of VMA21 as a potent actor in X-linked myopathy with excessive autophagy pathogenesis.

D-mannose acts as a V-ATPase inhibitor to suppress inflammatory cytokines generation and bacterial killing in macrophage.

The resolution of phagosomes.

TMEM175: A lysosomal ion channel associated with neurological diseases.

Nanosensor-based monitoring of autophagy-associated lysosomal acidification in vivo.

Deacidification of endolysosomes by neuronal aging drives synapse loss.

The pH-sensing Rim101 pathway regulates cell size in budding yeast.

Chimeric a-subunit isoforms generate functional yeast V-ATPases with altered regulatory properties in vitro and in vivo.

CLCN7, a gene shared by autosomal recessive and autosomal dominant osteopetrosis.

Subunit C of V-ATPase-VmaC Is Required for Hyphal Growth and Conidiation in A. fumigatus by Affecting Vacuolar Calcium Homeostasis and Cell Wall Integration.

ATP6V0C variants impair V-ATPase function causing a neurodevelopmental disorder often associated with epilepsy.

Vacuolar H+ -ATPase subunit VAB3 regulates cell growth and ion homeostasis in Arabidopsis.

Expanding the phenotype of ATP6AP1 deficiency.

Silencing of multiple target genes via ingestion of dsRNA and PMRi affects development and survival in Helicoverpa armigera.

Phenotypic and genetic spectrum of ATP6V1A encephalopathy: a disorder of lysosomal homeostasis.

Pathogen-induced autophagy regulates monolignol transport and lignin formation in plant immunity.

Astrocytic Glutamatergic Transmission and Its Implications in Neurodegenerative Disorders.

ATP6AP2 knockdown in cardiomyocyte deteriorates heart function via compromising autophagic flux and NLRP3 inflammasome activation.

HPS6 Regulates the Biogenesis of Weibel-Palade Body in Endothelial Cells Through Trafficking v-ATPase to Its Limiting Membrane.

Disruption of PIKFYVE causes congenital cataract in human and zebrafish.

Vacuolar (H+ )-ATPase subunit c is essential for the survival and systemic RNA interference response in Locusta migratoria.

Ion Channels and Pumps in Autophagy: A Reciprocal Relationship.

Variants in ATP6V0A1 cause progressive myoclonus epilepsy and developmental and epileptic encephalopathy.

miR-1 sustains muscle physiology by controlling V-ATPase complex assembly.

Defective Lipid Droplet-Lysosome Interaction Causes Fatty Liver Disease as Evidenced by Human Mutations in TMEM199 and CCDC115.

Congenital disorder of glycosylation caused by mutation of ATP6AP1 gene (c.1036G>A) in a Chinese infant: A case report.

A Novel Neuron-Specific Regulator of the V-ATPase in Drosophila.

Plasma Membrane Receptors Involved in the Binding and Response of Osteoclasts to Noncellular Components of the Bone.

RORα Enhances Lysosomal Acidification and Autophagic Flux in the Hepatocytes.

An auxin signaling network translates low-sugar-state input into compensated cell enlargement in the fugu5 cotyledon.

Vacuolar H+-ATPase dysfunction rescues intralumenal vesicle cargo sorting in yeast lacking PI(3,5)P2 or Doa4.

Genetic architecture and phenotypic landscape of deafness and onychodystrophy syndromes.

Vph1 is associated with the copper homeostasis of Cryptococcus neoformans serotype D.

Loss of zebrafish atp6v1e1b, encoding a subunit of vacuolar ATPase, recapitulates human ARCL type 2C syndrome and identifies multiple pathobiological signatures.

V-Type ATPase Mediates Airway Surface Liquid Acidification in Pig Small Airway Epithelial Cells.

Neurodegeneration Upon Dysfunction of Endosomal/Lysosomal CLC Chloride Transporters.

Ammonium Accumulation Caused by Reduced Tonoplast V-ATPase Activity in Arabidopsis thaliana.

The Ncoa7 locus regulates V-ATPase formation and function, neurodevelopment and behaviour.

Expanding the clinical and molecular spectrum of ATP6V1A related metabolic cutis laxa.

The V-ATPase regulates localization of the TRP Ca2+ channel Yvc1 in response to oxidative stress in Candida albicans.

Kinetic Separation of Oxidative and Non-oxidative Metabolism in Single Phagosomes from Alveolar Macrophages: Impact on Bacterial Killing.

Callyspongiolide Is a Potent Inhibitor of the Vacuolar ATPase.

Golgi pH and Ion Homeostasis in Health and Disease.

Knockdown of Tcirg1 inhibits large-osteoclast generation by down-regulating NFATc1 and IP3R2 expression.

Lysosomal activity regulates Caenorhabditis elegans mitochondrial dynamics through vitamin B12 metabolism.

C5a impairs phagosomal maturation in the neutrophil through phosphoproteomic remodeling.

Sugary Logistics Gone Wrong: Membrane Trafficking and Congenital Disorders of Glycosylation.

Screening for abnormal glycosylation in a cohort of adult liver disease patients.

Live imaging of intra-lysosome pH in cell lines and primary neuronal culture using a novel genetically encoded biosensor.

ALS/FTD mutations in UBQLN2 impede autophagy by reducing autophagosome acidification through loss of function.

Regulation and function of V-ATPases in physiology and disease.

Vacuolar H+ -ATPase is involved in preventing heavy metal-induced oxidative stress in Saccharomyces cerevisiae.

The conserved microRNA miR-8-3p coordinates the expression of V-ATPase subunits to regulate ecdysone biosynthesis for Drosophila metamorphosis.

Mutations in the V-ATPase Assembly Factor VMA21 Cause a Congenital Disorder of Glycosylation With Autophagic Liver Disease.

Screening and function discussion of a hereditary renal tubular acidosis family pathogenic gene.

RabX1 Organizes a Late Endosomal Compartment that Forms Tubular Connections to Lysosomes Consistent with a "Kiss and Run" Mechanism.

V-ATPase a3 isoform mutations identified in osteopetrosis patients abolish its expression and disrupt osteoclast function.

Carboxylated gold nanoparticles inhibit bone erosion by disturbing the acidification of an osteoclast absorption microenvironment.

Cysteine Toxicity Drives Age-Related Mitochondrial Decline by Altering Iron Homeostasis.

A rare case of autosomal recessive ATP6V0A4 variant of distal renal tubular acidosis in a young female with recurrent nephrolithiasis.

C9orf72 and smcr8 mutant mice reveal MTORC1 activation due to impaired lysosomal degradation and exocytosis.

Altered in vitro muscle differentiation in X-linked myopathy with excessive autophagy.

Observations From a Mouse Model of Forebrain Voa1 Knockout: Focus on Hippocampal Structure and Function.

Loss of Oxidation Resistance 1, OXR1, Is Associated with an Autosomal-Recessive Neurological Disease with Cerebellar Atrophy and Lysosomal Dysfunction.

An ECM-to-Nucleus Signaling Pathway Activates Lysosomes for C. elegans Larval Development.

Biallelic DMXL2 mutations impair autophagy and cause Ohtahara syndrome with progressive course.

Two tonoplast proton pumps function in Arabidopsis embryo development.

Nirogacestat suppresses RANKL-Induced osteoclast formation in vitro and attenuates LPS-Induced bone resorption in vivo.

Novel c.G630A TCIRG1 mutation causes aberrant splicing resulting in an unusually mild form of autosomal recessive osteopetrosis.

Spinocerebellar Ataxia Type 28-Phenotypic and Molecular Characterization of a Family with Heterozygous and Compound-Heterozygous Mutations in AFG3L2.

Targeting V-ATPase Isoform Restores Cisplatin Activity in Resistant Ovarian Cancer: Inhibition of Autophagy, Endosome Function, and ERK/MEK Pathway.

Cln3-mutations underlying juvenile neuronal ceroid lipofuscinosis cause significantly reduced levels of Palmitoyl-protein thioesterases-1 (Ppt1)-protein and Ppt1-enzyme activity in the lysosome.

Interaction of the late endo-lysosomal lipid PI(3,5)P2 with the Vph1 isoform of yeast V-ATPase increases its activity and cellular stress tolerance.

Functional complementation reveals that 9 of the 13 human V-ATPase subunits can functionally substitute for their yeast orthologs.

Vph2 is required for protection against a reductive stress in Candida albicans.

PSEN2 (presenilin 2) mutants linked to familial Alzheimer disease impair autophagy by altering Ca2+ homeostasis.

Chaperone-Mediated Autophagy Upregulation Rescues Megalin Expression and Localization in Cystinotic Proximal Tubule Cells.

Distinct Mycobacterium marinum phosphatases determine pathogen vacuole phosphoinositide pattern, phagosome maturation, and escape to the cytosol.

Comparative Genomic Screen in Two Yeasts Reveals Conserved Pathways in the Response Network to Phenol Stress.

Vacuolar hydrolysis and efflux: current knowledge and unanswered questions.

Decoding the Regulatory Logic of the Drosophila Male Stem Cell System.

Incomplete Distal Renal Tubular Acidosis and Kidney Stones.

V-ATPase-dependent repression of androgen receptor in prostate cancer cells.

ADM Scaffolds Generate a Pro-regenerative Microenvironment During Full-Thickness Cutaneous Wound Healing Through M2 Macrophage Polarization via Lamtor1.

Lgl reduces endosomal vesicle acidification and Notch signaling by promoting the interaction between Vap33 and the V-ATPase complex.

ATG5 overexpression is neuroprotective and attenuates cytoskeletal and vesicle-trafficking alterations in axotomized motoneurons.

PI(3,5)P2 controls vacuole potassium transport to support cellular osmoregulation.

The effect of V-ATPase function defects in pathogenesis of Alzheimer's disease.

ZnT2 is critical for lysosome acidification and biogenesis during mammary gland involution.

NAFLD Phenotype in Patients With V-ATPase Proton Pump Assembly Defects.

De novo mutations of the ATP6V1A gene cause developmental encephalopathy with epilepsy.

Histone deacetylase-mediated regulation of endolysosomal pH.

Intravesicular Acidification Regulates Lipopolysaccharide Inflammation and Tolerance through TLR4 Trafficking.

Vacuolar ATPase is required for ERK-dependent wound healing in the Drosophila embryo.

Mutations in ATP6AP2 cause autophagic liver disease in humans.

Molecular mechanisms of cutis laxa- and distal renal tubular acidosis-causing mutations in V-ATPase a subunits, ATP6V0A2 and ATP6V0A4.

Changes in V-ATPase subunits of human urinary exosomes reflect the renal response to acute acid/alkali loading and the defects in distal renal tubular acidosis.

Systemic RNAi of V-ATPase subunit B causes molting defect and developmental abnormalities in Periplaneta fuliginosa.

Identification and in silico characterization of a novel p.P208PfsX1 mutation in V-ATPase a3 subunit associated with autosomal recessive osteopetrosis in a Pakistani family.

Mammary epithelium-specific inactivation of V-ATPase reduces stiffness of extracellular matrix and enhances metastasis of breast cancer.

Mutations in the X-linked ATP6AP2 cause a glycosylation disorder with autophagic defects.

Cellular v-ATPase is required for virion assembly compartment formation in human cytomegalovirus infection.

F-actin reorganization by V-ATPase inhibition in prostate cancer.

Vma3p protects cells from programmed cell death through the regulation of Hxk2p expression.

Contribution of VMA5 to vacuolar function, stress response, ion homeostasis and autophagy in Candida albicans.

The synergistic effects of Sr and Si bioactive ions on osteogenesis, osteoclastogenesis and angiogenesis for osteoporotic bone regeneration.

Cardiac complications of congenital disorders of glycosylation (CDG): a systematic review of the literature.

Fructose-1,6-bisphosphate and aldolase mediate glucose sensing by AMPK.

The F-actin modulator SWAP-70 controls podosome patterning in osteoclasts.

Identification of Cerebral Metal Ion Imbalance in the Brain of Aging Octodon degus.

V-ATPases Containing a3 Subunit Play a Direct Role in Enamel Development in Mice.

Misrouting of v-ATPase subunit V0a1 dysregulates lysosomal acidification in a neurodegenerative lysosomal storage disease model.

Cellular vacuolization caused by overexpression of the PIKfyve-binding deficient Vac14L156R is rescued by starvation and inhibition of vacuolar-ATPase.

Functional coupling of V-ATPase and CLC-5.

The amino acid transporter SLC36A4 regulates the amino acid pool in retinal pigmented epithelial cells and mediates the mechanistic target of rapamycin, complex 1 signaling.

Mutations in ATP6V1E1 or ATP6V1A Cause Autosomal-Recessive Cutis Laxa.

Effect of vacuolar ATPase subunit H (VmaH) on cellular pH, asexual cycle, stress tolerance and virulence in Beauveria bassiana.

Deficiency of ATP6V1H Causes Bone Loss by Inhibiting Bone Resorption and Bone Formation through the TGF-β1 Pathway.

Cardiac autophagic vacuolation in severe X-linked myopathy with excessive autophagy.

Drosophila WASH is required for integrin-mediated cell adhesion, cell motility and lysosomal neutralization.

Autolysosome biogenesis and developmental senescence are regulated by both Spns1 and v-ATPase.

Renal Atp6ap2/(Pro)renin Receptor Is Required for Normal Vacuolar H+-ATPase Function but Not for the Renin-Angiotensin System.

Polarization of M2 macrophages requires Lamtor1 that integrates cytokine and amino-acid signals.

Roles of vacuolar H+-ATPase in the oxidative stress response of Candida glabrata.

The Function of V-ATPases in Cancer.

Active vacuolar H+ ATPase and functional cycle of Rab5 are required for the vacuolation defect triggered by PtdIns(3,5)P2 loss under PIKfyve or Vps34 deficiency.

ATP6AP1 deficiency causes an immunodeficiency with hepatopathy, cognitive impairment and abnormal protein glycosylation.

Disorders of lysosomal acidification-The emerging role of v-ATPase in aging and neurodegenerative disease.

N-Linked Glycosylation Is Required for Vacuolar H+ -ATPase (V-ATPase) a4 Subunit Stability, Assembly, and Cell Surface Expression.

A pure chloride channel mutant of CLC-5 causes Dent's disease via insufficient V-ATPase activation.

CCDC115 Deficiency Causes a Disorder of Golgi Homeostasis with Abnormal Protein Glycosylation.

TMEM199 Deficiency Is a Disorder of Golgi Homeostasis Characterized by Elevated Aminotransferases, Alkaline Phosphatase, and Cholesterol and Abnormal Glycosylation.

Ceramide signaling targets the PP2A-like protein phosphatase Sit4p to impair vacuolar function, vesicular trafficking and autophagy in Isc1p deficient cells.

Alteration of complex sphingolipid composition and its physiological significance in yeast Saccharomyces cerevisiae lacking vacuolar ATPase.

Conditional depletion of intellectual disability and Parkinsonism candidate gene ATP6AP2 in fly and mouse induces cognitive impairment and neurodegeneration.

8-Dehydrosterols induce membrane traffic and autophagy defects through V-ATPase dysfunction in Saccharomyces cerevisae.

Lysosomes: Regulators of autophagy in the retinal pigmented epithelium.

Tfp1 is required for ion homeostasis, fluconazole resistance and N-Acetylglucosamine utilization in Candida albicans.

The V-ATPase accessory protein Atp6ap1b mediates dorsal forerunner cell proliferation and left-right asymmetry in zebrafish.

Bafilomycin A1 disrupts autophagic flux by inhibiting both V-ATPase-dependent acidification and Ca-P60A/SERCA-dependent autophagosome-lysosome fusion.

Vacuolar ATPase depletion affects mitochondrial ATPase function, kinetoplast dependency, and drug sensitivity in trypanosomes.

Autophagosome-lysosome fusion is independent of V-ATPase-mediated acidification.

Regulation of lipid droplet dynamics in Saccharomyces cerevisiae depends on the Rab7-like Ypt7p, HOPS complex and V1-ATPase.

Discovery of a Small-Molecule Probe for V-ATPase Function.

V-ATPase activity in the TGN/EE is required for exocytosis and recycling in Arabidopsis.

Multiple functions of the SNARE protein Snap29 in autophagy, endocytic, and exocytic trafficking during epithelial formation in Drosophila.