ArticleScientific reports2015
Impaired ATP6V0A2 expression contributes to Golgi dispersion and glycosylation changes in senescent cells.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- Distinct roles of COPI proteins attenuated in cell senescence.Science advances · 2026Article
- Intercompartmental communication in senescence.FEBS open bio · 2026Review
- Metabolic changes in the one-carbon metabolism-related amino acids during etoposide-induced cellular senescence of neuronal cells.Cytotechnology · 2025Article
- Golgi pH homeostasis stabilizes the lysosomal membrane throughLife science alliance · 2024Article
- The different roles of V-ATPase a subunits in phagocytosis/endocytosis and autophagy.Autophagy · 2024Article
- High-throughput mechanical phenotyping and transcriptomics of single cells.Nature communications · 2024Article
- Identification of a novel intronic variant of ATP6V0A2 in a Han-Chinese family with cutis laxa.Molecular biology reports · 2024Article
- Review
- Exploring the Communication of the SASP: Dynamic, Interactive, and Adaptive Effects on the Microenvironment.International journal of molecular sciences · 2023Review
- Supply chain logistics - the role of the Golgi complex in extracellular matrix production and maintenance.Journal of cell science · 2022Review
- Why Should Natural Principles Be Simple?Philosophia (Ramat-Gan, Israel) · 2022Article
- Tankyrase-1-mediated degradation of Golgin45 regulates glycosyltransferase trafficking and protein glycosylation in Rab2-GTP-dependent manner.Communications biology · 2021Article
- Loss of zebrafish atp6v1e1b, encoding a subunit of vacuolar ATPase, recapitulates human ARCL type 2C syndrome and identifies multiple pathobiological signatures.PLoS genetics · 2021Article
- Review
- Conditional Deletion of the V-ATPase a2-Subunit Disrupts Intrathymic T Cell Development.Frontiers in immunology · 2019Article
- Delphinidin-3-glucoside suppresses lipid accumulation in HepG2 cells.Cytotechnology · 2018Article
- A versatile drug delivery system targeting senescent cells.EMBO molecular medicine · 2018Article
- Mammary epithelium-specific inactivation of V-ATPase reduces stiffness of extracellular matrix and enhances metastasis of breast cancer.Molecular oncology · 2018Article
- SMARCD1 regulates senescence-associated lipid accumulation in hepatocytes.NPJ aging and mechanisms of disease · 2017Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many genes and signaling pathways have been found to be involved in cellular senescence program. In the present study, we have identified 16 senescence-associated genes by differential proteomic analysis of the normal human diploid fibroblast cell line, TIG-1, and focused on ATP6V0A2. The aim of this study is to clarify the role of ATP6V0A2, the causal gene for ARCL2, a syndrome of abnormal glycosylation and impaired Golgi trafficking, in cellular senescence program. Here we showed that ATP6V0A2 is critical for cellular senescence; impaired expression of ATP6V0A2 disperses the Golgi structure and triggers senescence, suggesting that ATP6V0A2 mediates these processes. FITC-lectin staining and glycoblotting revealed significantly different glycosylation structures in presenescent (young) and senescent (old) TIG-1 cells; reducing ATP6V0A2 expression in young TIG-1 cells yielded structures similar to those in old TIG-1 cells. Our results suggest that senescence-associated impaired expression of ATP6V0A2 triggers changes in Golgi structure and glycosylation in old TIG-1 cells, which demonstrates a role of ATP6V0A2 in cellular senescence program.
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