ArticleScientific reports2020
Deletion of the GAPDH gene contributes to genome stability in Saccharomyces cerevisiae.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Yeast Chronological Lifespan Model as a Tool for Screening Aging Interventions.International journal of molecular sciences · 2026Review
- RNA binding of GAPDH controls transcript stability and protein translation in acute myeloid leukemia.RNA biology · 2025Article
- Transcriptional Regulation Mechanisms in Adaptively EvolvedJournal of fungi (Basel, Switzerland) · 2025Article
- Epigenetic mechanisms of particulate matter exposure: air pollution and hazards on human health.Frontiers in genetics · 2023Review
- Review
- The role of NAD and NAD precursors on longevity and lifespan modulation in the budding yeast, Saccharomyces cerevisiae.Biogerontology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular metabolism is directly or indirectly associated with various cellular processes by producing a variety of metabolites. Metabolic alterations may cause adverse effects on cell viability. However, some alterations potentiate the rescue of the malfunction of the cell system. Here, we found that the alteration of glucose metabolism suppressed genome instability caused by the impairment of chromatin structure. Deletion of the TDH2 gene, which encodes glyceraldehyde 3-phospho dehydrogenase and is essential for glycolysis/gluconeogenesis, partially suppressed DNA damage sensitivity due to chromatin structure, which was persistently acetylated histone H3 on lysine 56 in cells with deletions of both HST3 and HST4, encoding NAD
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Registered trials
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