ArticleNature communications2024
The chromatin factors SET-26 and HCF-1 oppose the histone deacetylase HDA-1 in longevity and gene regulation in C. elegans.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 8 citations in OpenAlex.
- A somatic checkpoint through NHR-49/HNF4α governs reproductive investment and longevity in C. elegans.Nature communications · 2026Article
- RBFOX1 association with age at onset of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- A SET domain-containing protein and HCF-1 maintain transgenerational epigenetic memory.Nature communications · 2026Article
- Nuclear Hormone Receptor NHR-49/HNF4α Couples Fertility Regulation to Resource Allocation and Longevity inbioRxiv : the preprint server for biology · 2025Article
- Chromatin and epigenetics in aging biology.Genetics · 2025Review
- SUMO-mediated regulation of H3K4me3 reader SET-26 controls germline development in C. elegans.PLoS biology · 2025Article
- Immunotherapies for Aging and Age-Related Diseases: Advances, Pitfalls, and Prospects.Research (Washington, D.C.) · 2025Review
- CanPharmaceuticals (Basel, Switzerland) · 2024Review
- Chromatin: the old and young of it.Frontiers in molecular biosciences · 2023Review
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6 authors at 3 institutions in 3 countries.
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Abstract
SET-26, HCF-1, and HDA-1 are highly conserved chromatin factors with key roles in development and aging. Here we present mechanistic insights into how these factors regulate gene expression and modulate longevity in C. elegans. We show that SET-26 and HCF-1 cooperate to regulate a common set of genes, and both antagonize the histone deacetylase HDA-1 to limit longevity. HCF-1 localization at chromatin is largely dependent on functional SET-26, whereas SET-26 is only minorly affected by loss of HCF-1, suggesting that SET-26 could recruit HCF-1 to chromatin. HDA-1 opposes SET-26 and HCF-1 on the regulation of a subset of their common target genes and in longevity. Our findings suggest that SET-26, HCF-1, and HDA-1 comprise a mechanism to fine-tune gene expression and longevity and likely have important implications for the mechanistic understanding of how these factors function in diverse organisms, particularly in aging biology.
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