Affinage

ATP6V1G1

V-type proton ATPase subunit G 1 · UniProt O75348

Length
118 aa
Mass
13.8 kDa
Annotated
2026-04-28
38 papers in source corpus 17 papers cited in narrative 17 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ATP6V1G1 encodes the G1 subunit of the V-ATPase peripheral stalk and is essential for V1-V0 domain assembly, ATP hydrolysis, and proton-pumping activity required for lysosomal, endosomal, and autophagosomal acidification (PMID:7775427, PMID:9099722, PMID:41432243). N-terminal residues of the G subunit stabilize its heterodimerization with the E subunit and control the reversible association of the V1 catalytic sector with the V0 membrane sector, a key regulatory step modulated by ATM kinase–mediated phosphorylation of ATP6V1G1, which disrupts E–G dimerization and impairs lysosomal function (PMID:10969085, PMID:28346404). RILP directs ATP6V1G1 to late endosomal membranes and controls its turnover through ubiquitin-dependent proteasomal degradation, thereby linking Rab7 activation and endosomal pH sensing to V-ATPase assembly in a feedback circuit (PMID:24762812, PMID:38578235). ATP6V1G1 expression is regulated transcriptionally by RORα, post-transcriptionally by FTO-dependent m6A demethylation and by a TDMD site that degrades miR-335-3p, and at the protein level by UBQLN2, whose ALS/FTD-linked mutations destabilize ATP6V1G1 and compromise autophagic flux (PMID:34558854, PMID:41191778, PMID:41871909, PMID:32513711).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1995 High

    Establishing that the small G/Vma10p subunit is a stoichiometric V-ATPase component required for V1 sector assembly onto the membrane and for vacuolar acidification resolved the identity and essential role of this previously uncharacterized polypeptide.

    Evidence Yeast VMA10 null mutant phenotyping (quinacrine uptake, neutral pH growth), protein purification and sequencing

    PMID:7775427

    Open questions at the time
    • Copy number per holoenzyme not precisely determined
    • No high-resolution structural data
  2. 1997 High

    Reconstitution of ATPase activity from purified recombinant subunits including G1 demonstrated that G1 is directly required for catalysis in the V1 sector, not merely for structural integrity.

    Evidence In vitro reconstitution of ATPase activity from recombinant A, B, C, E, and G1 subunits expressed in E. coli/Sf9 cells

    PMID:9099722

    Open questions at the time
    • Precise catalytic contribution of G1 versus structural scaffolding not separated
    • Structural basis of G1 alpha-helical fold predicted but not solved
  3. 2000 High

    Systematic mutagenesis of the G subunit N-terminus revealed that specific residues control E subunit stability and the reversibility of V1-V0 association, identifying the G subunit as a regulatory determinant of glucose-dependent disassembly.

    Evidence Site-directed mutagenesis of yeast Vma10p (R25A/L, Y46A, K55A), growth assays, V-ATPase assembly and glucose-deprivation disassembly analysis

    PMID:10969085

    Open questions at the time
    • Mammalian G1 residues not directly mutagenized
    • Molecular contacts between G and E not resolved at atomic level
  4. 2014 High

    Discovery that RILP directly binds ATP6V1G1, controls its membrane recruitment, and regulates its ubiquitylation and proteasomal degradation established the first post-translational regulatory axis controlling V-ATPase assembly through G1 subunit turnover.

    Evidence Yeast two-hybrid, reciprocal co-immunoprecipitation, ubiquitylation assays, proteasome inhibitor experiments, lysosomal acidification readout

    PMID:24762812

    Open questions at the time
    • Identity of the E3 ubiquitin ligase mediating G1 ubiquitylation not determined
    • Whether RILP-G1 interaction is direct at endogenous stoichiometric levels in all cell types
  5. 2017 High

    Identification of ATM kinase as a direct phosphorylation-dependent inhibitor of E–G dimerization and V1-V0 assembly linked DNA damage response signaling to lysosomal dysfunction and provided a mechanistic basis for senescence-associated lysosomal defects.

    Evidence In vitro ATM kinase assay on ATP6V1G1, co-immunoprecipitation of E-G dimers ± ATM inhibitor, LysoTracker lysosomal pH assay

    PMID:28346404

    Open questions at the time
    • Specific phosphorylation site(s) on G1 not mapped
    • Structural consequence of phosphorylation on E-G interface not resolved
  6. 2020 High

    Demonstration that UBQLN2 stabilizes ATP6V1G1 protein levels and that ALS/FTD-associated UBQLN2 mutations reduce this interaction, impairing autophagosome acidification, connected V-ATPase G1 regulation to neurodegenerative disease pathogenesis.

    Evidence In vitro pulldown, UBQLN2-KO HeLa cells, ATP6V1G1 overexpression rescue of acidification and autophagic flux

    PMID:32513711

    Open questions at the time
    • Whether UBQLN2 protects G1 from ubiquitin-proteasome degradation or acts through another mechanism not fully delineated
    • In vivo neuronal validation not provided
  7. 2021 Medium

    Oxidized ATM phosphorylation of ATP6V1G1 in cancer-associated fibroblasts diverts autophagosome flux toward exosome secretion, extending the ATM-G1 axis from senescence to the tumor microenvironment and paracrine signaling.

    Evidence ATM inhibitor and shRNA in fibroblasts, lysosomal acidification, autophagosome tracking, exosome quantification, cancer cell invasion assay

    PMID:34545708

    Open questions at the time
    • Direct phosphorylation of G1 by oxidized ATM not independently confirmed beyond prior Kang et al. study
    • Contribution of G1 phosphorylation versus other ATM substrates not isolated
  8. 2021 Medium

    Identification of RORα as a transcriptional inducer of Atp6v1g1 in hepatocytes established a transcription-level regulatory input controlling V-ATPase acidification capacity and downstream autophagic flux in a metabolic context.

    Evidence Hepatocyte-specific RORα KO mouse, adenoviral RORα overexpression, LysoSensor assay, cathepsin D maturation

    PMID:34558854

    Open questions at the time
    • Direct RORα binding to the Atp6v1g1 promoter not demonstrated by ChIP
    • Whether other V-ATPase subunits are co-regulated not addressed
  9. 2024 High

    Establishing a V-ATPase–RILP–Rab7 feedback loop on late endosomes, where luminal pH neutralization increases G1-containing V-ATPase assembly and hyperactivates Rab7, revealed how organelle pH is sensed and transduced into membrane trafficking decisions.

    Evidence pH neutralization (LLOMe, NH4Cl), proximity ligation assay for V1G1 assembly, dominant-active Rab7 mutants, CI-M6PR tubulation assay

    PMID:38578235

    Open questions at the time
    • Whether V-ATPase directly senses pH or responds to downstream signals not resolved
    • Generalizability beyond CI-M6PR cargo sorting not tested
  10. 2024 Medium

    In vivo gain-of-function and loss-of-function experiments in microglia and MPTP-treated mice showed that ATP6V1G1 levels control α-synuclein clearance via lysosomal acidification, positioning G1 as a neuroprotective factor in Parkinson's disease models.

    Evidence PD patient exosome treatment, siRNA knockdown, lentiviral ATP6V1G1 overexpression in mouse brain, MPTP model behavioral and histological analysis

    PMID:38702933

    Open questions at the time
    • Mechanism by which PD exosomes reduce G1 expression not identified
    • Single mouse model; not confirmed in genetic PD models
  11. 2025 Medium

    Discovery that FTO-dependent m6A demethylation sustains ATP6V1G1 expression and that this is required for lysosomal autophagy during ABC B-cell differentiation added epitranscriptomic regulation to the multi-layered control of G1 abundance.

    Evidence FTO KO/overexpression in B cells, m6A modification analysis, V-ATPase activity assay, mitochondrial and autophagy flux assays, ABC differentiation readout

    PMID:41191778

    Open questions at the time
    • Specific m6A sites on ATP6V1G1 mRNA not mapped
    • Whether FTO acts directly on G1 mRNA or indirectly through other targets not fully resolved
  12. 2025 Medium

    Identification of a TDMD site in the Atp6v1g1 3' UTR that directs miR-335-3p degradation revealed a non-canonical regulatory function of this mRNA beyond protein coding, linking it to miRNA homeostasis.

    Evidence Computational prediction, mouse genetic site-deletion models, CLASH-based miRNA-target mapping, small RNA sequencing in Zswim8−/− mice

    PMID:41871909

    Open questions at the time
    • Functional consequence of miR-335-3p stabilization on V-ATPase activity or cellular phenotype not tested
    • Whether the TDMD function is conserved in humans not demonstrated
  13. 2026 High

    Heart-specific ATP6V1G1 knockout confirmed the subunit is indispensable for V-ATPase assembly and proton-pumping in cardiomyocytes, directly linking G1 loss to impaired endo-lysosomal acidification and autophagy block analogous to lipotoxic stress.

    Evidence Cardiac-specific KO mouse, fractionation, proximity ligation assay, colorimetric proton-pumping assay, autophagy flux analysis

    PMID:41432243

    Open questions at the time
    • Whether cardiac phenotype leads to heart failure or cardiomyopathy not described
    • Compensatory roles of G2 or G3 isoforms not assessed

Open questions

Synthesis pass · forward-looking unresolved questions
  • The precise phosphorylation site(s) on ATP6V1G1 targeted by ATM, the identity of the E3 ubiquitin ligase mediating RILP-dependent G1 degradation, and the structural basis of how G1 modifications alter E–G dimerization and V1-V0 coupling remain unresolved.
  • ATM phosphorylation site on G1 unmapped
  • E3 ligase for G1 ubiquitylation unknown
  • High-resolution structure of mammalian E-G heterodimer with post-translational modifications lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0140657 ATP-dependent activity 3
Localization
GO:0005764 lysosome 5 GO:0005768 endosome 2 GO:0031410 cytoplasmic vesicle 2 GO:0005773 vacuole 1
Pathway
R-HSA-9612973 Autophagy 5 R-HSA-382551 Transport of small molecules 4 R-HSA-5653656 Vesicle-mediated transport 2 R-HSA-8953854 Metabolism of RNA 1
Complex memberships
V-ATPase (V1 sector)V-ATPase holoenzyme (V1-V0)

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
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

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 Chemical screening identifies ATM as a target for alleviating senescence. Nature chemical biology 148 28346404
2005 Distinct expression patterns of different subunit isoforms of the V-ATPase in the rat epididymis. Biology of reproduction 141 16192400
2021 Hypoxia-stimulated ATM activation regulates autophagy-associated exosome release from cancer-associated fibroblasts to promote cancer cell invasion. Journal of extracellular vesicles 107 34545708
2002 Identification of I kappa BL as the second major histocompatibility complex-linked susceptibility locus for rheumatoid arthritis. American journal of human genetics 100 12509789
2001 A second susceptibility gene for developing rheumatoid arthritis in the human MHC is localized within a 70-kb interval telomeric of the TNF genes in the HLA class III region. Genomics 88 11170743
1995 The Saccharomyces cerevisiae VMA10 is an intron-containing gene encoding a novel 13-kDa subunit of vacuolar H(+)-ATPase. The Journal of biological chemistry 81 7775427
2002 Systematic identification of the genes affecting glycogen storage in the yeast Saccharomyces cerevisiae: implication of the vacuole as a determinant of glycogen level. Molecular & cellular proteomics : MCP 80 12096123
2020 ALS/FTD mutations in UBQLN2 impede autophagy by reducing autophagosome acidification through loss of function. Proceedings of the National Academy of Sciences of the United States of America 70 32513711
2014 RILP regulates vacuolar ATPase through interaction with the V1G1 subunit. Journal of cell science 65 24762812
2015 The vacuolar H+ ATPase is a novel therapeutic target for glioblastoma. Oncotarget 52 26020805
1997 Subunit G of the vacuolar proton pump. Molecular characterization and functional expression. The Journal of biological chemistry 52 9099722
2000 Mutational analysis of subunit G (Vma10p) of the yeast vacuolar H+-ATPase. The Journal of biological chemistry 48 10969085
1997 The intriguing evolution of the "b" and "G" subunits in F-type and V-type ATPases: isolation of the vma-10 gene from Neurospora crassa. Journal of bioenergetics and biomembranes 32 9559854
2014 A new V-ATPase regulatory mechanism mediated by the Rab interacting lysosomal protein (RILP). Communicative & integrative biology 27 26843904
2024 Iron metabolism disorder and multiple sclerosis: a comprehensive analysis. Frontiers in immunology 23 38590521
2015 Bivariate Genome-Wide Association Study Implicates ATP6V1G1 as a Novel Pleiotropic Locus Underlying Osteoporosis and Age at Menarche. The Journal of clinical endocrinology and metabolism 23 26312577
2021 RORα Enhances Lysosomal Acidification and Autophagic Flux in the Hepatocytes. Hepatology communications 21 34558854
2020 Proteomic Characterization of Proliferation Inhibition of Well-Differentiated Laryngeal Squamous Cell Carcinoma Cells Under Below-Background Radiation in a Deep Underground Environment. Frontiers in public health 18 33194991
2023 Disturbance of gut microbiota aggravates cadmium-induced neurotoxicity in zebrafish larvae through V-ATPase. The Science of the total environment 12 37245817
2018 Genomic regions and enrichment analyses associated with carcass composition indicator traits in Nellore cattle. Journal of animal breeding and genetics = Zeitschrift fur Tierzuchtung und Zuchtungsbiologie 11 30592105
2024 Collapse of late endosomal pH elicits a rapid Rab7 response via the V-ATPase and RILP. Journal of cell science 10 38578235
2024 Identification and validation of cuproptosis and disulfidptosis related genes in colorectal cancer. Cellular signalling 9 38643947
2000 Cloning and expression of cDNAs encoding plant V-ATPase subunits in the corresponding yeast null mutants. Biochimica et biophysica acta 8 11004467
2002 Does the rat have an H2-D orthologue next to Bat1? Immunogenetics 7 11904681
2020 Interplay Between V-ATPase G1 and Small EV-miRNAs Modulates ERK1/2 Activation in GBM Stem Cells and Nonneoplastic Milieu. Molecular cancer research : MCR 6 32753475
2016 Methylation and expression analyses of Pallister-Killian syndrome reveal partial dosage compensation of tetrasomy 12p and hypomethylation of gene-poor regions on 12p. Epigenetics 6 26890086
2024 Plasma exosomes impair microglial degradation of α-synuclein through V-ATPase subunit V1G1. CNS neuroscience & therapeutics 5 38702933
2024 Proteomic Analysis Reveals Oxidative Phosphorylation and JAK-STAT Pathways Mediated Pathogenesis of Pemphigus Vulgaris. Experimental dermatology 5 39373252
2025 Identification of shared genetic loci for asthma, allergic rhinitis, and pollinosis in East Asians. Scientific reports 4 39972113
1998 Organellar H(+)-ATPase--site directed mutagenesis and suppressor mutants. Acta physiologica Scandinavica. Supplementum 3 9789560
2025 CLASHub: an integrated database and analytical platform for microRNA-target interactions. bioRxiv : the preprint server for biology 2 40799581
2025 The m6A demethylase FTO links TLR7 to mitochondrial oxidation driving age-associated B cell formation in systemic lupus erythematosus. Science translational medicine 2 41191778
2025 mRNA 3' UTRs direct microRNA degradation to participate in imprinted gene networks and regulate growth. bioRxiv : the preprint server for biology 2 41279844
2024 Identification and characterization of the receptors of a microneme adhesive repeat domain of Eimeria maxima microneme protein 3 in chicken intestine epithelial cells. Poultry science 2 38350385
2026 Comprehensive methodological evaluation of V-ATPase assembly in the context of cardiac lipid overload: implications for (endo)lysosomal function and autophagy. Autophagy 0 41432243
2026 mRNA 3' UTRs direct microRNA degradation to participate in imprinted gene networks and regulate growth. Genes & development 0 41871909
2025 Analysis of the toxicity and mechanisms of osteoporosis caused by cigarette toxicants using network toxicology and molecular docking techniques. The Science of the total environment 0 40925315
2025 Evolution of the Chick Embryo Chorioallantoic Membrane Proteome during Early Development. ACS omega 0 41552518