Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automatic assignment of GO terms using logical inference, based on on inter-ontology links
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Integral and associated lysosomal membrane proteins.
Large-scale proteomics and phosphoproteomics of urinary exosomes.
Proteomic analysis of human parotid gland exosomes by multidimensional protein identification technology (MudPIT).
MHC class II-associated proteins in B-cell exosomes and potential functional implications for exosome biogenesis.
mTORC1 senses lysosomal amino acids through an inside-out mechanism that requires the vacuolar H(+)-ATPase.
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V-ATPase (V1A subunit confirmed to co-immunoprecipitate with Ragulator) is required for amino acid-induced mTORC1 activation at the lysosome.
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V1 domain interacts with Ragulator in an amino acid-sensitive manner.
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ATP hydrolysis by V-ATPase is required for the amino acid signaling but the proton gradient itself is not.
Lipofuscin is formed independently of macroautophagy and lysosomal activity in stress-induced prematurely senescent human fibroblasts.
Vacuolar-type H+-ATPase V1A subunit is a molecular partner of Wolfram syndrome 1 (WFS1) protein, which regulates its expression and stability.
In-depth proteomic analyses of exosomes isolated from expressed prostatic secretions in urine.
The vacuolar-ATPase complex and assembly factors, TMEM199 and CCDC115, control HIF1α prolyl hydroxylation by regulating cellular iron levels.
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ATP6V1A depletion by CRISPR stabilizes HIF1α under aerobic conditions.
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Mechanism is via intracellular iron depletion impairing PHD activity, not direct lysosomal degradation of HIF1α.
De novo mutations of the ATP6V1A gene cause developmental encephalopathy with epilepsy.
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Four de novo heterozygous ATP6V1A mutations cause IECEE3.
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Mutations disrupt lysosomal homeostasis and neuronal development.
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V-ATPase plays specific roles in neurotransmitter loading and synaptic connectivity.
Structure and Roles of V-type ATPases.
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Comprehensive review of V-ATPase structure, function, and disease associations.
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V-ATPase is the primary organellar acidification system in eukaryotes.
Structures of a Complete Human V-ATPase Reveal Mechanisms of Its Assembly.
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First complete human V-ATPase cryo-EM structure at 2.9 Angstrom resolution.
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ATP6V1A is the catalytic A subunit; three copies form the catalytic AB hexameric ring.
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Identifies mechanisms of V-ATPase assembly involving ATP6AP1, glycans, and lipids.
The ATPase ATP6V1A facilitates rabies virus replication by promoting virion uncoating and interacting with the viral matrix protein.
Identification of two subunit A isoforms of the vacuolar H(+)-ATPase in human osteoclastoma.
Intraphagosomal pH is lowered to 5 by V-ATPase
Acidification of Tf:TfR1 containing endosome
RRAGC,D exchanges GTP for GDP
RRAGA,B exchanges GDP for GTP
v-ATPase:Ragulator:RRAGA,B:GTP:RRAGC,D:GDP:SLC38A9:Arginine dissociates yielding v-ATPase:Ragulator:RRAGA,B:GTP:RRAGC,D:GDP and SLC38A9:Arginine
v-ATPase:Ragulator:RagA,B:GDP:RagC,D:GDP binds SLC38A9:Arginine
v-ATPase:Ragulator:RRAGA,B:GTP:RRAGC,D:GDP binds mTORC1
MITF-M-dependent ATP6V1A gene expression