ArticleGenes2021
Set1 Targets Genes with Essential Identity and Tumor-Suppressing Functions in Planarian Stem Cells.
Article in Genes, 2021. 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.
The trial behind it
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- A dynamic histone-based chromatin regulatory toolkit underpins genome and developmental evolution in an invertebrate clade.Genome biology · 2025Article
- Chromatin remodeling protein BPTF mediates chromatin accessibility at gene promoters in planarian stem cells.BMC genomics · 2025Article
- A comparative analysis of planarian genomes reveals regulatory conservation in the face of rapid structural divergence.Nature communications · 2024Article
- Purification of Planarian Stem Cells Using a Draq5-Based FACS Approach.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Functional genomics in Spiralia.Briefings in functional genomics · 2023Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Tumor suppressor genes (TSGs) are essential for normal cellular function in multicellular organisms, but many TSGs and tumor-suppressing mechanisms remain unknown. Planarian flatworms exhibit particularly robust tumor suppression, yet the specific mechanisms underlying this trait remain unclear. Here, we analyze histone H3 lysine 4 trimethylation (H3K4me3) signal across the planarian genome to determine if the broad H3K4me3 chromatin signature that marks essential cell identity genes and TSGs in mammalian cells is conserved in this valuable model of in vivo stem cell function. We find that this signature is indeed conserved on the planarian genome and that the lysine methyltransferase Set1 is largely responsible for creating it at both cell identity and putative TSG loci. In addition, we show that depletion of
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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.