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ATP6V0C

V-type proton ATPase 16 kDa proteolipid subunit c · UniProt P27449

Length
155 aa
Mass
15.7 kDa
Annotated
2026-06-09
33 papers in source corpus 15 papers cited in narrative 15 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ATP6V0C encodes the proteolipid c-subunit of the V0 membrane domain of the vacuolar H+-ATPase, where it is indispensable for assembly of the complex (including the a and b subunits) and for the proton pumping that acidifies the vacuolar/lysosomal lumen, supporting vacuolar biogenesis, protein transport, and endocytosis (PMID:2145283, PMID:23913543). It is the bafilomycin A1-binding subunit of the neuronal V-ATPase, and its loss raises lysosomal pH, blocks autophagic flux at the lysosomal degradation step, and causes accumulation of α-synuclein species and APP C-terminal fragments (PMID:24695574); beyond this acidification role, ATP6V0C acts as a scaffold that bridges the SNARE proteins STX17 and VAMP8 to mediate autophagosome-lysosome fusion, with its expression directly driven by TFEB (PMID:38481802). Through control of intracellular and extracellular pH it governs MMP-2/MMP-9 activation and tumor invasion/metastasis (PMID:16061667, PMID:29138865) and lysosomal pH-dependent sequestration of chemotherapeutic drugs (PMID:19299075). ATP6V0C directly binds HIF-1α at its N-terminus, competing with VHL to stabilize HIF-1α and form a positive feedback loop that drives pathology in acute lung injury (PMID:17178925, PMID:41738275), and its abundance is restrained by RNF182-mediated ubiquitin-proteasome degradation (PMID:18298843). Heterozygous ATP6V0C variants that impair V-ATPase function cause a human neurodevelopmental/epileptic disorder, modeled across yeast, Drosophila, and C. elegans (PMID:36074901). It is also hijacked by pathogens, interacting with HIV-1 Vpu to promote tetherin degradation (PMID:32291285) and forming an HRG-1 complex required for parasite heme acquisition (PMID:41838682), and transgenic expression promotes retinal ganglion cell survival and axon regeneration (PMID:42023031).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1990 High

    Established that the c-subunit is not merely structural but genetically essential for V-ATPase activity, complex assembly, and downstream acidification-dependent cell biology.

    Evidence VMA3 gene disruption in S. cerevisiae with ATPase activity, in vivo acidification, endocytosis, and subunit-assembly assays

    PMID:2145283

    Open questions at the time
    • Done in yeast ortholog; human subunit assembly contribution inferred
    • Atomic mechanism of how c-subunit nucleates a/b assembly not resolved
  2. 2002 High

    Defined how ATP6V0C transcription is controlled, identifying cooperative Sp1/Oct1 promoter occupancy as the basis for drug-induced, anti-apoptotic V-ATPase induction.

    Evidence Genomic cloning, in vivo footprinting, EMSA, promoter-reporter and site-directed mutagenesis assays

    PMID:12133827

    Open questions at the time
    • Signaling upstream of Sp1/Oct1 recruitment not mapped
    • Generality beyond topoisomerase-inhibitor stress unclear
  3. 2005 High

    Connected ATP6V0C proton secretion to a malignant phenotype, showing it controls intracellular pH recovery, MMP-2 activation, and metastasis.

    Evidence Stable siRNA knockdown in hepatocellular carcinoma, pH measurement, zymography, Matrigel invasion, and xenograft assays

    PMID:16061667

    Open questions at the time
    • Mechanistic link between pH change and MMP-2 transcription/activation not dissected
    • Whether plasma-membrane vs lysosomal V-ATPase pool drives invasion unresolved
  4. 2006 Medium

    Revealed a non-canonical role: direct binding to HIF-1α competing with VHL to stabilize and co-translocate HIF-1α, linking V-ATPase to hypoxia signaling.

    Evidence siRNA, overexpression, reciprocal co-IP, confocal microscopy, and HIF-1α domain mapping

    PMID:17178925

    Open questions at the time
    • Single lab; structural basis of the ATP6V0C–HIF-1α interface undefined
    • How a membrane proteolipid reaches nuclear HIF-1α mechanistically unclear
  5. 2008 Medium

    Identified post-translational control of ATP6V0C abundance through RNF182-mediated ubiquitination and proteasomal degradation.

    Evidence Yeast two-hybrid screen, in vitro/in vivo co-precipitation, E3 ligase and proteasome degradation assays

    PMID:18298843

    Open questions at the time
    • Ubiquitination sites on ATP6V0C not mapped
    • Physiological conditions triggering RNF182-dependent turnover unknown
  6. 2009 Medium

    Demonstrated ATP6V0C governs chemoresistance by setting lysosomal pH that sequesters drugs away from the nucleus.

    Evidence siRNA knockdown in MCF-7/ADR cells, lysosomal pH and drug-distribution/cytotoxicity assays

    PMID:19299075

    Open questions at the time
    • Single lab; in vivo relevance to resistant tumors not tested
    • Quantitative contribution vs other resistance mechanisms unclear
  7. 2013 High

    Confirmed conserved essentiality of the c-subunit for V-ATPase assembly, proton transport, and virulence-associated secretion/filamentation in a fungal pathogen.

    Evidence Tetracycline-regulated VMA3 repression in C. albicans with ATPase, transport, pH, secretion, and epistasis assays

    PMID:23913543

    Open questions at the time
    • Direct molecular link between V-ATPase and filamentation regulators not established
    • Fungal-specific; human counterpart of secretion phenotype untested
  8. 2014 High

    Placed ATP6V0C at the lysosomal degradation step of autophagy in neurons, showing its loss impairs flux and accumulates neurodegeneration-associated substrates.

    Evidence siRNA in differentiated SH-SY5Y cells, LysoTracker, LC3/LAMP-1 co-localization, substrate Western blots, neurite measurement

    PMID:24695574

    Open questions at the time
    • Distinguished flux block from fusion defect here but mechanism of substrate selectivity unclear
    • Causality for in vivo neurodegeneration not addressed
  9. 2017 Medium

    Extended the invasion role to prostate cancer and linked ATP6V0C to plasma-membrane LASS2/TMSG1 in a feedback relationship.

    Evidence siRNA, V-ATPase activity, extracellular pH, MMP-9 zymography, invasion/migration, and co-localization assays

    PMID:29138865

    Open questions at the time
    • Nature of ATP6V0C–LASS2/TMSG1 regulation not mechanistically defined
    • Invasion effect shown LASS2-independent but alternate effector unidentified
  10. 2020 Medium

    Showed pathogen exploitation: ATP6V0C interacts with HIV-1 Vpu and is required for Vpu-mediated tetherin degradation and viral release.

    Evidence Yeast two-hybrid, siRNA in HeLa, overexpression, immunofluorescence, HIV-1 release and tetherin Western assays

    PMID:32291285

    Open questions at the time
    • Whether interaction requires assembled V-ATPase or free c-subunit unclear
    • Trafficking step where tetherin is routed for degradation not pinpointed
  11. 2023 High

    Established ATP6V0C as a human disease gene, with heterozygous variants impairing acidification and producing neurological phenotypes across model species.

    Evidence Patient variants tested by yeast complementation, in silico modelling, Drosophila knockdown seizure, and C. elegans variant-expression assays

    PMID:36074901

    Open questions at the time
    • Variant effects on the human complex not directly measured
    • Mechanism linking acidification deficit to seizures undefined
  12. 2024 Medium

    Separated ATP6V0C's scaffolding function from its pump function, showing it bridges STX17/VAMP8 for autophagosome-lysosome fusion and is a direct TFEB target.

    Evidence CUT&Run-qPCR, luciferase reporter, co-IP with STX17/VAMP8, AAV9-TFEB in UUO mouse model, autophagic flux assays

    PMID:38481802

    Open questions at the time
    • Structural basis of SNARE bridging unresolved
    • How scaffold and pump roles are partitioned within the same molecule unclear
  13. 2026 High

    Confirmed in vivo the ATP6V0C–HIF-1α positive feedback loop as a driver of acute lung injury.

    Evidence Alveolar-specific Atp6v0c and Hif1a conditional knockouts, co-IP, transcriptomics, AAV overexpression in LPS-induced ALI model

    PMID:41738275

    Open questions at the time
    • Direct transcription-factor mechanism by which HIF-1α induces ATP6V0C not detailed
    • Whether feedback operates in other inflammatory tissues untested
  14. 2026 Medium

    Identified an additional pathogen-cofactor role, with the parasite ATP6V0C–HRG-1 complex required for heme acquisition and development.

    Evidence HRG-1/ATP6V0C interaction studies, RNAi, bafilomycin inhibition, heme uptake and mouse infection assays in T. spiralis

    PMID:41838682

    Open questions at the time
    • Whether heme transport depends on acidification or direct complex function unclear
    • Parasite ortholog; human heme-transport relevance untested
  15. 2026 Medium

    Demonstrated therapeutic potential, with ATP6V0C overexpression promoting RGC survival and axon regeneration after optic nerve injury.

    Evidence AAV2 Atp6v0c transgene, optic nerve crush model, RGC survival and axon regeneration quantification

    PMID:42023031

    Open questions at the time
    • Proposed lysosomal/ER-stress mechanism not directly tested
    • Single study; dependence on V-ATPase activity vs scaffold role unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single proteolipid subunit partitions between proton-pumping, SNARE-scaffolding, HIF-1α-binding, and pathogen-cofactor functions, and the structural basis of its non-canonical interactions, remains unresolved.
  • No structural model of ATP6V0C bound to HIF-1α or STX17/VAMP8
  • Whether moonlighting functions require assembled V-ATPase or free subunit unknown
  • Mechanism connecting acidification loss to specific neurological phenotypes undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 3 GO:0005198 structural molecule activity 1 GO:0060090 molecular adaptor activity 1
Localization
GO:0005764 lysosome 3 GO:0005773 vacuole 2 GO:0005634 nucleus 1 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 2 R-HSA-382551 Transport of small molecules 2 R-HSA-9612973 Autophagy 2 R-HSA-5653656 Vesicle-mediated transport 1
Partners
ATP6V0AHIF1AHRG-1LASS2/TMSG1RNF182STX17VAMP8
Complex memberships
vacuolar H+-ATPase (V0 domain)

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1990 The VMA3 gene product (subunit c of vacuolar H+-ATPase, ortholog of ATP6V0C) is essential for vacuolar H+-ATPase activity and vacuolar acidification in vivo; deletion of VMA3 abolishes ATPase activity and the subunit c is indispensable for assembly of subunits a and b of the H+-ATPase complex. Loss of VMA3 also impairs vacuolar biogenesis, protein transport to the vacuole, and completely inhibits endocytosis. VMA3 gene disruption in S. cerevisiae, measurement of vacuolar ATPase activity, in vivo acidification assay, endocytosis assay with lucifer yellow CH, subunit assembly analysis The Journal of biological chemistry High 2145283
2002 The ATP6V0C promoter contains four GC boxes and an Oct1-binding site occupied by Sp1 and Oct1 in vivo. Cooperative binding of Sp1 and Oct1 to the promoter is required for transcriptional activation by the topoisomerase II inhibitor TAS-103, while cisplatin regulates ATP6L expression post-transcriptionally via mRNA stability. Induction of V-ATPase expression acts as an anti-apoptotic defense. Genomic cloning, in vivo footprint analysis, promoter-reporter assays, site-directed mutagenesis of Oct1 site, electrophoretic mobility shift assay (EMSA), RT-PCR for mRNA stability The Journal of biological chemistry High 12133827
2005 Knockdown of ATP6L (ATP6V0C) using siRNA in highly metastatic hepatocellular carcinoma cells inhibits proton secretion, intracellular pH recovery from acidification, reduces MMP-2 expression and gelatinase activity, suppresses invasion in vitro, and dramatically reduces tumor growth and metastasis in vivo in a xenograft mouse model. DNA vector-based siRNA stable transfection, intracellular pH measurement, Matrigel invasion assay, gelatin zymography, nude mouse xenograft implantation Cancer research High 16061667
2006 ATP6V0C directly interacts with HIF-1α through the N-terminal end (amino acids 1-16) of HIF-1α, competing with Von Hippel-Lindau protein for HIF-1α binding. ATP6V0C overexpression increases HIF-1α levels in a gene dose-dependent manner, and bafilomycin A1 stimulates this interaction and causes co-translocation of ATP6V0C with HIF-1α from the cytoplasm to the nucleus. ATP6V0C knockdown by siRNA, overexpression, co-immunoprecipitation, confocal immunofluorescence microscopy, HIF-1α domain mapping Molecular pharmacology Medium 17178925
2008 The E3 ubiquitin ligase RNF182 directly interacts with ATP6V0C (identified by yeast two-hybrid screening and confirmed by co-precipitation in vitro and in vivo) and targets ATP6V0C for degradation via the ubiquitin-proteasome pathway. Yeast two-hybrid screening, overexpression and co-precipitation (in vitro and in vivo), E3 ligase activity assay, proteasome degradation assay Molecular neurodegeneration Medium 18298843
2009 Knockdown of ATP6L (ATP6V0C) in drug-resistant breast cancer cells (MCF-7/ADR) increases lysosomal pH and causes retention of anticancer drugs (doxorubicin, 5-fluorouracil, vincristine) in nuclei rather than sequestration in acidic lysosomes, sensitizing cells to chemotherapy. This identifies V-ATPase c subunit as a regulator of intracellular pH-dependent drug distribution. siRNA knockdown, qRT-PCR, Western blot, lysosomal pH measurement, drug distribution/nuclear retention assay, cytotoxicity assay Cancer letters Medium 19299075
2013 In Candida albicans, VMA3 repression prevents V-ATPase assembly at the vacuolar membrane, reduces concanamycin A-sensitive ATPase activity and proton transport by >90%, alkalinizes the vacuolar lumen, impairs aspartyl protease and lipase secretion, and suppresses filamentation. V-ATPase-dependent filamentation defects are not rescued by overexpression of RIM8, MDS3, EFG1, CST20, or UME6, suggesting V-ATPase functions downstream or independently of these regulators. Conditional tetracycline-regulated promoter replacement, ATPase activity assay, proton transport assay, vacuolar pH measurement, vacuolar morphology analysis, secretion assays, genetic epistasis with filamentation regulators Eukaryotic cell High 23913543
2014 ATP6V0C is the bafilomycin A1-binding subunit of vacuolar ATPase in neuronal cells. Knockdown of ATP6V0C reduces lysosomal acidity (LysoTracker staining), increases basal LC3-II levels, α-synuclein high molecular weight species, and APP C-terminal fragments, inhibits autophagic flux, and reduces neurite length. Enhanced LC3/LAMP-1 co-localization indicates the autophagic flux block occurs at the lysosomal degradation step, not at vesicular fusion. siRNA knockdown in differentiated SH-SY5Y cells, quantitative RT-PCR, LysoTracker Red staining, immunofluorescence (LC3/LAMP-1 co-localization), Western blot for LC3-II/α-synuclein/APP-CTF, neurite length measurement, propidium iodide viability assay PloS one High 24695574
2017 Silencing of ATP6V0C in highly metastatic prostate cancer cells inhibits V-ATPase activity (~5-fold), decreases extracellular hydrogen ion concentration, reduces activation of secreted MMP-9 (~3.6-fold), and inhibits cell migration and invasion. ATP6V0C co-localizes with LASS2/TMSG1 at the plasma membrane, and silencing ATP6V0C reduces LASS2/TMSG1 expression, suggesting a feedback regulatory relationship. The invasion suppression is not LASS2/TMSG1-dependent. siRNA knockdown, V-ATPase activity assay, extracellular pH measurement, gelatin zymography (MMP-9 activation), Matrigel invasion assay, wound migration assay, confocal immunofluorescence co-localization Oncology reports Medium 29138865
2020 ATP6V0C interacts with HIV-1 accessory protein Vpu (identified by yeast two-hybrid screening). ATP6V0C depletion by knockdown impairs Vpu-mediated tetherin degradation and results in defective HIV-1 release. ATP6V0C overexpression stabilizes tetherin expression and sequesters it in CD63/LAMP1-positive intracellular compartments. This effect is specific to ATP6V0C, as overexpression of ATP6V0C″ (another V-ATPase subunit) had no effect on tetherin. Yeast two-hybrid screening, siRNA knockdown in HeLa cells, overexpression, immunofluorescence localization, HIV-1 release assay, Western blot for tetherin The Journal of biological chemistry Medium 32291285
2023 Heterozygous point variants in ATP6V0C impair V-ATPase function: functional analyses in S. cerevisiae showed reduced LysoSensor fluorescence (decreased vacuolar acidification) and reduced growth in CaCl2-containing media. In silico modelling indicated variants interfere with ATP6V0C–ATP6V0A subunit interactions during ATP hydrolysis. Knockdown of ATP6V0C in Drosophila increased duration of seizure-like behaviour, and expression of patient variants in C. elegans led to reduced growth, motor dysfunction, and reduced lifespan. Patient variant identification, yeast functional complementation assay (LysoSensor fluorescence, calcium sensitivity growth assay), in silico structural modelling, Drosophila knockdown seizure assay, C. elegans variant expression with behavioral/viability assays Brain : a journal of neurology High 36074901
2024 TFEB directly binds the ATP6V0C promoter at a specific site to transcriptionally activate ATP6V0C expression, as demonstrated by CUT&Run-qPCR and luciferase reporter assay. ATP6V0C acts as a scaffold protein that mediates autophagosome-lysosome fusion by bridging with STX17 and VAMP8 (SNARE complex), independently of its role in lysosomal acidification/degradation. Loss of TFEB in renal fibrosis reduces ATP6V0C expression, impairing autophagic flux and causing tubular cell G2/M arrest. RNA-seq, CUT&Tag, CUT&Run-qPCR, luciferase reporter assay, co-immunoprecipitation (ATP6V0C with STX17 and VAMP8), AAV9-TFEB overexpression in UUO mouse model, autophagic flux assay International journal of biological sciences Medium 38481802
2026 ATP6V0C and HIF-1α form a positive feedback loop in acute lung injury: ATP6V0C interacts with HIF-1α (confirmed by co-immunoprecipitation), HIF-1α transcriptionally regulates ATP6V0C expression, and ATP6V0C in turn promotes HIF-1α upregulation. Alveolar-specific ATP6V0C knockout mice show attenuated LPS-induced acute lung injury (reduced inflammation and epithelial apoptosis), and overexpression of ATP6V0C exacerbates ALI in a HIF-1α-dependent manner. Alveolar-specific conditional knockout (Atp6v0cAT2-KO), HIF-1α knockout (Hif1aAT2-KO), co-immunoprecipitation, transcriptomic analysis, AAV-mediated overexpression, LPS-induced ALI model American journal of respiratory cell and molecular biology High 41738275
2026 In T. spiralis, the HRG-1/ATP6V0C complex is essential for heme acquisition by the parasite. Ts-ATP6V0C interacts with Ts-HRG-1 to form a functional complex required for heme transport. RNAi knockdown of Ts-ATP6V0C or inhibition by bafilomycin A1 impairs heme uptake, causes developmental arrest, and reduces larval burden in mouse hosts. Protein-protein interaction studies (HRG-1/ATP6V0C complex), RNAi knockdown of Ts-ATP6V0C, bafilomycin A1 inhibition, heme uptake assay, in vivo mouse infection model PLoS pathogens Medium 41838682
2026 Atp6v0c transgene expression in retinal ganglion cells (via AAV2 intravitreal injection) promotes RGC survival and long-distance axon regeneration after optic nerve crush, comparable in efficacy to targeting Pten and Klf9. This identifies ATP6V0C as an axon regeneration-promoting factor, likely through support of lysosomal acidification and degradation of misfolded proteins in response to ER stress in injured neurons. AAV2-mediated Atp6v0c transgene expression, optic nerve crush model in rodents, RGC survival quantification, axon regeneration measurement Molecular therapy. Nucleic acids Medium 42023031

Source papers

Stage 0 corpus · 33 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 The growth and metastasis of human hepatocellular carcinoma xenografts are inhibited by small interfering RNA targeting to the subunit ATP6L of proton pump. Cancer research 130 16061667
1990 Roles of the VMA3 gene product, subunit c of the vacuolar membrane H(+)-ATPase on vacuolar acidification and protein transport. A study with VMA3-disrupted mutants of Saccharomyces cerevisiae. The Journal of biological chemistry 122 2145283
2002 Enhanced expression of the human vacuolar H+-ATPase c subunit gene (ATP6L) in response to anticancer agents. The Journal of biological chemistry 70 12133827
2009 Small interfering RNA targeting the subunit ATP6L of proton pump V-ATPase overcomes chemoresistance of breast cancer cells. Cancer letters 68 19299075
2014 ATP6V0C knockdown in neuroblastoma cells alters autophagy-lysosome pathway function and metabolism of proteins that accumulate in neurodegenerative disease. PloS one 54 24695574
2008 A novel brain-enriched E3 ubiquitin ligase RNF182 is up regulated in the brains of Alzheimer's patients and targets ATP6V0C for degradation. Molecular neurodegeneration 53 18298843
2013 Candida albicans VMA3 is necessary for V-ATPase assembly and function and contributes to secretion and filamentation. Eukaryotic cell 39 23913543
2006 ATP6V0C competes with von Hippel-Lindau protein in hypoxia-inducible factor 1alpha (HIF-1alpha) binding and mediates HIF-1alpha expression by bafilomycin A1. Molecular pharmacology 27 17178925
2023 ATP6V0C variants impair V-ATPase function causing a neurodevelopmental disorder often associated with epilepsy. Brain : a journal of neurology 26 36074901
2018 A new microdeletion syndrome involving TBC1D24, ATP6V0C, and PDPK1 causes epilepsy, microcephaly, and developmental delay. Genetics in medicine : official journal of the American College of Medical Genetics 25 30245510
2018 Bcl-2-dependent synthetic lethal interaction of the IDF-11774 with the V0 subunit C of vacuolar ATPase (ATP6V0C) in colorectal cancer. British journal of cancer 22 30420612
2022 ATP6V0C Is Associated With Febrile Seizures and Epilepsy With Febrile Seizures Plus. Frontiers in molecular neuroscience 20 35600075
2024 Impaired TFEB-mediated autophagy-lysosome fusion promotes tubular cell cycle G2/M arrest and renal fibrosis by suppressing ATP6V0C expression and interacting with SNAREs. International journal of biological sciences 18 38481802
2019 High glucose disrupts autophagy lysosomal pathway in gingival epithelial cells via ATP6V0C. Journal of periodontology 17 31471894
2017 Silencing of vacuolar ATPase c subunit ATP6V0C inhibits the invasion of prostate cancer cells through a LASS2/TMSG1-independent manner. Oncology reports 16 29138865
2020 Haploinsufficiency of ATP6V0C possibly underlies 16p13.3 deletions that cause microcephaly, seizures, and neurodevelopmental disorder. American journal of medical genetics. Part A 13 33090716
2020 ATP6L promotes metastasis of colorectal cancer by inducing epithelial-mesenchymal transition. Cancer science 12 31840304
1994 The proteolipid subunit of the Neurospora crassa vacuolar ATPase: isolation of the protein and the vma-3 gene. Molecular & general genetics : MGG 12 8190074
2020 The viral protein U (Vpu)-interacting host protein ATP6V0C down-regulates cell-surface expression of tetherin and thereby contributes to HIV-1 release. The Journal of biological chemistry 9 32291285
2020 Novel de novo mutation substantiates ATP6V0C as a gene causing epilepsy with intellectual disability. Brain & development 8 33190975
2009 Refined genomic localization of the genetic lesion in the osteopetrosis (op) rat and exclusion of three positional and functional candidate genes, Clcn7, Atp6v0c, and Slc9a3r2. Calcified tissue international 7 19259722
2002 Chromosomal localization of three vacuolar-H+ -ATPase 16 kDa subunit (ATP6V0C) genes in the murine genome. Cytogenetic and genome research 6 12438748
2001 Expression of V-ATPase proteolipid subunit of Acetabularia acetabulum in a VMA3-deficient strain of Saccharomyces cerevisiae and its complementation study. European journal of biochemistry 6 11733003
2025 Variants in ATP6V0C are associated with Dravet-like developmental and epileptic encephalopathy. Epilepsia 4 40085430
2023 ATP6V0C gene variants were identified in individuals with epilepsy, with or without developmental delay. Journal of human genetics 2 37161035
2017 Specification of binding modes between a transmembrane peptide mimic of ATP6V0C and polytopic E5 of human papillomavirus-16. Journal of biomolecular structure & dynamics 2 28786342
2025 Mechanistic insights into 16p13.3 microdeletions encompassing TBC1D24 and ATP6V0C through advanced sequencing approaches. European journal of human genetics : EJHG 1 40721525
2019 [Novel tumor metastasis suppressorgene LASS2/TMSG1 S248A mutant promotes invasion of prostate cancer cells through increasing ATP6V0C expression]. Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences 1 30996356
2017 [Silencing of vacuolar ATPase c subunit ATP6V0C inhibits invasion of prostate cancer cells]. Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences 1 29263462
2026 ATP6V0C-HIF-1α reciprocal activation drives acute lung injury. American journal of respiratory cell and molecular biology 0 41738275
2026 Bafilomycin A1 is a promising therapeutic agent against T. spiralis infection by inhibiting the heme-transporting ATP6V0C/HRG-1 complex. PLoS pathogens 0 41838682
2026 Vacuolar ATPase subunit Atp6v0c transgene promotes neuroprotection and long-distance axon regeneration in injured retinal ganglion neurons. Molecular therapy. Nucleic acids 0 42023031
2002 Functional expression of Acetabularia acetabulum vacuolar H(+)-pyrophosphatase in a yeast VMA3-deficient strain. Journal of experimental botany 0 12379795

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