ArticleNature medicine2010
Modulation of histone H3 lysine 56 acetylation as an antifungal therapeutic strategy.
Article in Nature medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.
- Meta-analysis of niacin and NAD metabolite treatment in infectious disease animal studies suggests benefit but requires confirmation in clinically relevant models.Scientific reports · 2025Pooled it
- Antifungal resistance: from classical mechanisms to the expanding role of acetyltransferases.Journal of biomedical science · 2026Review
- Genetic and Epigenetic Mechanisms Underlying Reversible Adaptive Responses in Fungi.Journal of fungi (Basel, Switzerland) · 2026Review
- Review
- Investigating the pH dependent antifungal effects of butyrate onFrontiers in microbiology · 2026Article
- Disruptive DNA Intercalation Is the Mode of Interaction Behind Niacinamide Antimicrobial Activity.Microorganisms · 2025Article
- Core histones govern echinocandin susceptibility inMicrobiology spectrum · 2025Article
- Targeting epigenetic regulators to overcome drug resistance in the emerging human fungal pathogen Candida auris.Nature communications · 2025Article
- Potential role of lysine acetylation in the stepwise adaptation ofMicrobiology spectrum · 2025Article
- Antifungal drug resistance in Candida glabrata: role of cellular signaling and gene regulatory networks.FEMS yeast research · 2025Review
- Article
- Protein lysine acetylation regulates oral microorganisms.Frontiers in cellular and infection microbiology · 2025Review
- Repurposing Plant-Based Histone Acetyltransferase Inhibitors: A Review of Novel Therapeutic Strategies Against Drug-Resistant Fungal Biofilms.Current microbiology · 2024Review
- Niacinamide Antimicrobial Efficacy and Its Mode of Action via Microbial Cell Cycle Arrest.Microorganisms · 2024Article
- Histone acetyltransferase Sas3 contributes to fungal development, cell wall integrity, and virulence inApplied and environmental microbiology · 2024Article
- Two sirtuin proteins, Hst3 and Hst4, modulate asexual development, stress tolerance, and virulence by affecting global gene expression inMicrobiology spectrum · 2024Article
- Old and new strategies in therapy and diagnosis against fungal infections.Applied microbiology and biotechnology · 2024Review
- Multiple micronutrient deficiencies in early life cause multi-kingdom alterations in the gut microbiome and intrinsic antibiotic resistance genes in mice.Nature microbiology · 2023Article
- Post-transcriptional control of antifungal resistance in human fungal pathogens.Critical reviews in microbiology · 2023Review
- Morphogenic plasticity: the pathogenic attribute of Candida albicans.Current genetics · 2023Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Candida albicans is a major fungal pathogen that causes serious systemic and mucosal infections in immunocompromised individuals. In yeast, histone H3 Lys56 acetylation (H3K56ac) is an abundant modification regulated by enzymes that have fungal-specific properties, making them appealing targets for antifungal therapy. Here we demonstrate that H3K56ac in C. albicans is regulated by the RTT109 and HST3 genes, which respectively encode the H3K56 acetyltransferase (Rtt109p) and deacetylase (Hst3p). We show that reduced levels of H3K56ac sensitize C. albicans to genotoxic and antifungal agents. Inhibition of Hst3p activity by conditional gene repression or nicotinamide treatment results in a loss of cell viability associated with abnormal filamentous growth, histone degradation and gross aberrations in DNA staining. We show that genetic or pharmacological alterations in H3K56ac levels reduce virulence in a mouse model of C. albicans infection. Our results demonstrate that modulation of H3K56ac is a unique strategy for treatment of C. albicans and, possibly, other fungal infections.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.