ArticleThe EMBO journal2012
The histone methyltransferase Setd8 acts in concert with c-Myc and is required to maintain skin.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
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
53 citing papers in PubMed, 94 citations in OpenAlex.
- p63 in skin homeostasis and disease: molecular mechanisms and therapeutic potentials.Cell death discovery · 2026Review
- Epigenetic Regulation of Sebaceous and Meibomian Glands: From Development to Disease.Biomedicines · 2026Review
- Transcriptional and epigenetic mechanisms governing epidermal stem cell regulation.Frontiers in cell and developmental biology · 2026Review
- Multiple functions of the lysine methyltransferase KMT5a in cancer: potential targets for innovative therapies.Clinical epigenetics · 2025Review
- Unveiling the Role of Histone Methyltransferases in Psoriasis Pathogenesis: Insights from Transcriptomic Analysis.International journal of molecular sciences · 2025Article
- SUMOylation of SETD8 Promotes Tumor Growth by Methylating and Stabilizing MYC in Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Review
- Longevity cosmeceuticals as the next frontier in cosmetic innovation: a scientific framework for substantiating product claims.Frontiers in aging · 2025Review
- SETD8 inhibition targets cancer cells with increased rates of ribosome biogenesis.Cell death & disease · 2024Article
- PR-SET7 epigenetically restrains uterine interferon response and cell death governing proper postnatal stromal development.Nature communications · 2024Article
- Direct Lineage Reprogramming for Induced Keratinocyte Stem Cells: A Potential Approach for Skin Repair.Stem cells translational medicine · 2023Review
- Epigenetic Mechanisms of Epidermal Differentiation.International journal of molecular sciences · 2022Review
- Article
- Targeting the methyltransferase SETD8 impairs tumor cell survival and overcomes drug resistance independently of p53 status in multiple myeloma.Clinical epigenetics · 2021Article
- Epigenetic Regulation of Epidermal Differentiation.Epigenomes · 2021Review
- HDAC3 ensures stepwise epidermal stratification via NCoR/SMRT-reliant mechanisms independent of its histone deacetylase activity.Genes & development · 2020Article
- The histone methyltransferase Setd8 alters the chromatin landscape and regulates the expression of key transcription factors during erythroid differentiation.Epigenetics & chromatin · 2020Article
- Epigenetic control in skin development, homeostasis and injury repair.Experimental dermatology · 2019Review
- Targeting epigenetic mechanisms in diabetic wound healing.Translational research : the journal of laboratory and clinical medicine · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Setd8/PR-Set7/KMT5a-dependent mono-methylation of histone H4 at lysine 20 is essential for mitosis of cultured cells; yet, the functional roles of Setd8 in complex mammalian tissues are unknown. We use skin as a model system to explore how Setd8 may regulate cell division in vivo. Deletion of Setd8 in undifferentiated layers of the mouse epidermis impaired both proliferation and differentiation processes. Long-lived epidermal progenitor cells are lost in the absence of Setd8, leading to an irreversible loss of sebaceous glands and interfollicular epidermis. We show that Setd8 is a transcriptional target of c-Myc and an essential mediator of Myc-induced epidermal differentiation. Deletion of Setd8 in c-Myc-overexpressing skin blocks proliferation and differentiation and causes apoptosis. Increased apoptosis may be explained by our discovery that p63, an essential transcription factor for epidermal commitment is lost, while p53 is gained upon removal of Setd8. Both overexpression of p63 and deletion of p53 rescue Setd8-induced apoptosis. Thus, Setd8 is a crucial inhibitor of apoptosis in skin and its activity is essential for epidermal stem cell survival, proliferation and differentiation.
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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.