| 1995 |
The yeast VMA10 gene (ortholog of ATP6V1G1) encodes a 13-kDa subunit (M16/Vma10p) that copurifies with the V-ATPase complex, is present in multiple copies per enzyme, and is required for assembly of the catalytic V1 sector onto the vacuolar membrane; deletion causes loss of vacuolar acidification and failure to grow at neutral pH. |
Protein purification, amino acid sequencing, null mutant phenotyping (quinacrine accumulation, growth at pH 7.5), cold inactivation experiment placing Vma10p in the membrane sector |
The Journal of biological chemistry |
High |
7775427
|
| 1997 |
ATP6V1G1 (subunit G1) was purified from clathrin-coated vesicle V-ATPase, sequenced, and shown to be required for ATP hydrolysis; reconstitution of recombinant subunits A, B, C, E with recombinant G1 reconstituted ATPase activity, demonstrating G1's direct catalytic role in the V1 sector. |
Protein purification, direct sequencing, cDNA cloning, recombinant expression in E. coli and Sf9 cells, in vitro ATPase reconstitution assay |
The Journal of biological chemistry |
High |
9099722
|
| 1997 |
Sequence analysis of the Neurospora crassa G subunit (vma-10 ortholog) showed that the N-terminal half can form an alpha-helix with all conserved residues clustered on one face, supporting a stator stalk structural model analogous to the b subunit of F-ATPases but lacking a membrane-spanning region. |
Gene cloning, sequence analysis, structural modeling of conserved residues |
Journal of bioenergetics and biomembranes |
Medium |
9559854
|
| 2000 |
Site-directed mutagenesis of yeast Vma10p (ATP6V1G1 ortholog) showed that N-terminal residues (Y46, K55) are critical for stabilizing subunit E and V-ATPase assembly; R25A/R25L mutations stabilized V1-V0 association and partially prevented glucose-deprivation-induced disassembly while retaining full enzymatic activity; E14A and K50A allowed assembly but produced unstable complexes. |
Site-directed mutagenesis, growth assays at pH 7.5, V-ATPase assembly analysis, glucose-deprivation disassembly assay |
The Journal of biological chemistry |
High |
10969085
|
| 2005 |
ATP6V1G1 localizes to the apical pole of narrow and clear cells in rat epididymis and vas deferens, co-distributing with other V-ATPase subunits required for active proton secretion and luminal acidification, as determined by immunolocalization. |
Immunolocalization/immunofluorescence in epididymal tissue sections |
Biology of reproduction |
Medium |
16192400
|
| 2014 |
RILP (Rab7 effector) directly interacts with ATP6V1G1 (V1G1 subunit of V-ATPase) and controls its recruitment to late endosomal and lysosomal membranes, regulates V1G1 stability by promoting its ubiquitylation and proteasomal degradation, and thereby modulates V-ATPase assembly and activity; altered V1G1 expression impaired V-ATPase-dependent lysosomal acidification. |
Yeast two-hybrid, co-immunoprecipitation, pulldown, ubiquitylation assays, proteasome inhibitor experiments, V-ATPase activity assays, knockdown/overexpression with lysosomal acidification readout |
Journal of cell science |
High |
24762812
|
| 2015 |
ATP6V1G1 knockdown in glioblastoma neurospheres impaired sphere-forming ability, induced cell death, and decreased matrix invasion, phenocopied by bafilomycin A1 V-ATPase inhibition; this established ATP6V1G1-dependent V-ATPase activity as required for glioblastoma stem cell maintenance. |
siRNA knockdown, neurosphere formation assay, cell death assay, invasion assay, pharmacological inhibition with bafilomycin A1 |
Oncotarget |
Medium |
26020805
|
| 2017 |
ATM kinase directly interacts with V-ATPase V1 subunits ATP6V1E1 and ATP6V1G1 (identified by yeast two-hybrid), and ATM phosphorylates ATP6V1G1 to inhibit E-G dimerization; ATM inhibition restored dimerization, promoted V1-V0 domain assembly, and rescued lysosomal acidification, linking ATM activity to lysosomal dysfunction in senescence. |
Yeast two-hybrid screen, direct phosphorylation assay (ATM kinase assay on ATP6V1G1), co-immunoprecipitation of E-G dimerization, lysosomal acidification assay (LysoTracker), ATM inhibitor (KU-60019) treatment |
Nature chemical biology |
High |
28346404
|
| 2020 |
UBQLN2 binds ATP6V1G1 and regulates its expression and stability; ALS/FTD mutant UBQLN2 proteins bind ATP6V1G1 more weakly than wild-type, resulting in decreased ATP6V1G1 protein levels, impaired autophagosome acidification, and reduced autophagic flux; overexpression of ATP6V1G1 in UBQLN2-knockout cells restored autophagosome acidification. |
In vitro interaction/pulldown assay, proteomic analysis, immunoblot, UBQLN2 knockout HeLa cells, autophagy flux assay, lysosomal pH measurement, overexpression rescue experiment |
Proceedings of the National Academy of Sciences of the United States of America |
High |
32513711
|
| 2020 |
ATP6V1G1 (V1G1) expression in glioblastoma stem cells modulates the miRNA composition of secreted small extracellular vesicles; V1G1-high neurospheres release EVs that activate ERK1/2 signaling in recipient cells, and this oncogenic reprogramming is reversed by V-ATPase inhibition or forced expression of MAPK-targeting miRNAs. |
siRNA knockdown, EV isolation, miRNA profiling, ERK1/2 phosphorylation assay, proliferation/motility assays, pharmacological V-ATPase inhibition, miRNA overexpression |
Molecular cancer research : MCR |
Medium |
32753475
|
| 2021 |
Oxidized ATM (redox-activated, DNA-damage-independent) phosphorylates ATP6V1G1 in cancer-associated fibroblasts, causing lysosomal dysfunction; this diverts autophagosomes to fuse with multivesicular bodies rather than lysosomes, facilitating exosome release and promoting breast cancer cell invasion. |
ATM inhibitor (KU60019) treatment, shRNA knockdown of ATM and BNIP3, lysosomal acidification assay, autophagosome tracking, exosome quantification, cancer cell invasion assay |
Journal of extracellular vesicles |
Medium |
34545708
|
| 2021 |
RORα transcriptionally induces Atp6v1g1 expression to maintain lysosomal acidification in hepatocytes; hepatocyte-specific RORα deletion reduced lysosomal acidity and impaired autophagic flux, while adenoviral RORα overexpression increased lysosomal acidity. |
Hepatocyte-specific knockout mouse, adenoviral overexpression, LysoSensor assay, LC3-II/p62/NBR1 accumulation, cathepsin D maturation assay, mTOR lysosomal translocation |
Hepatology communications |
Medium |
34558854
|
| 2024 |
pH neutralization of late endosomes increases assembly of ATP6V1G1-containing V-ATPase on endosomal membranes, which stabilizes GTP-bound (active) Rab7 via RILP, leading to hyperactivation of Rab7 and disruption of CI-M6PR recycling tubulation; this defines a V-ATPase–RILP–Rab7 feedback pathway linking luminal pH to endosomal Rab7 activity. |
LLOMe treatment, NH4Cl pH neutralization, immunofluorescence, live imaging, proximity ligation assay for V1G1 assembly, dominant-active Rab7 mutants, CI-M6PR trafficking assay |
Journal of cell science |
High |
38578235
|
| 2024 |
PD patient-derived plasma exosomes decreased ATP6V1G1 expression in microglia, impairing lysosomal acidification and causing accumulation of swollen lysosomes with reduced cathepsin activity, leading to α-synuclein accumulation; lentiviral overexpression of ATP6V1G1 in the brain of MPTP-treated mice conferred neuroprotection. |
Exosome isolation and stereotaxic injection, LysoSensor pH measurement, immunofluorescence, western blotting, siRNA knockdown, lentiviral ATP6V1G1 overexpression, MPTP mouse model, rotarod/pole behavioral tests, TH immunostaining |
CNS neuroscience & therapeutics |
Medium |
38702933
|
| 2025 |
FTO (m6A demethylase), activated by TLR7-MyD88 signaling, promotes ABC B-cell differentiation by sustaining ATP6V1G1 expression in an m6A-dependent manner; FTO deficiency reduced ATP6V1G1-mediated V-ATPase activity, impairing lysosomal autophagy, causing damaged mitochondria to accumulate, and blocking ABC differentiation. |
FTO knockout/overexpression in murine and human B cells, m6A modification analysis, V-ATPase activity assay, lysosomal autophagy flux assay, mitochondrial function assays (OXPHOS, ROS), ABC differentiation assay |
Science translational medicine |
Medium |
41191778
|
| 2025 |
A TDMD (target-directed microRNA degradation) site in the 3' UTR of Atp6v1g1 mRNA directs the degradation of miR-335-3p in mouse models, acting in collaboration with two sites in Lpar4; this identifies ATP6V1G1 mRNA as a regulatory RNA whose 3' UTR participates in miRNA turnover. |
Computational prediction, mouse genetic models (site deletion), CLASH-based miRNA-target interaction, small RNA sequencing, miRNA quantification in Zswim8-/- mice |
Genes & development |
Medium |
41871909
|
| 2026 |
Heart-specific knockout of ATP6V1G1 in mice demonstrated that ATP6V1G1 is required for V-ATPase assembly and proton-pumping activity in cardiomyocytes; loss of ATP6V1G1 leads to impaired endo/lysosomal acidification and autophagy inhibition, recapitulating effects of high-fat diet-induced lipid overload. |
Heart-specific ATP6V1G1-knockout mouse model, fractionation, immunoprecipitation, proximity ligation assay, immunofluorescence, colorimetric proton-pumping assay, autophagy flux assay |
Autophagy |
High |
41432243
|