ArticleNeurochemical research2003
Genetic adaptation controlled by methylations and acetylations at the nuclear and cytosolic levels: a hypothetical model.
Article in Neurochemical research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed, 2 citations in OpenAlex.
- Cancer Metabolism: Fasting Reset, the Keto-Paradox and Drugs for Undoing.Journal of clinical medicine · 2023Review
- Synergistic effects of sodium butyrate, a histone deacetylase inhibitor, on increase of neurogenesis induced by pyridoxine and increase of neural proliferation in the mouse dentate gyrus.Neurochemical research · 2011Article
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1 author at 1 institution in 1 country.
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Abstract
Metabolic sensors related to the maturation of metabolism seem to control a process of generic adaptation involving the silencing of genes and the expression of their copies more adapted to environmental changes. Nuclear methylases and histone deacetylases control the gene silencing process. Nuclear methylases compete with cytosolic methylases for the same methyl donnors, this will favor the expression of unmethylated more adapted gene copies, when cytosotic methylases take over. Methylated cytosolic compounds may then represent an index of this adaptation. If a more adapted gene copy is mutated, the regulatory ligand of the gene product that does not find its target may induce a reexpression of the silenced gene. The hypothetical model proposed considers that gene silencing and expression of a more adequate copy involves a non-specific gene silencer switch that depends on the histone status; the silencer switch is counteracted by the ligand of the adapted gene copy product acting like an inducer.
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