ArticleNucleic acids research2018
Histone variant H2A.Z deposition and acetylation directs the canonical Notch signaling response.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- Set1 promotes Notch-induced transcriptional activation.Cellular and molecular life sciences : CMLS · 2026Article
- H2A.Z is essential for oocyte maturation and fertility in female mouse.Nature structural & molecular biology · 2025Article
- INO80/SWR remodelers regulate Pol II transcription through BRD2 and chromatin landscape.Nucleic acids research · 2025Article
- The Notch pathway: A guardian of cell fate during neurogenesis.Current opinion in cell biology · 2025Review
- The Drosophila histone variant H2Av facilitates Notch signaling activity in a two-tier regulatory fashion.Cell communication and signaling : CCS · 2025Article
- Copy Number Gains of VPS72 Drive De Novo Lipogenesis and Hepatocarcinogenesis via ATF3/mTORC1/SREBP1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pancreatic Cancer: Pathogenesis and Clinical Studies.MedComm · 2025Review
- Multifunctional histone variants in genome function.Nature reviews. Genetics · 2025Review
- The advances in acetylation modification in senescence and aging-related diseases.Frontiers in physiology · 2025Review
- ChIP-DIP maps binding of hundreds of proteins to DNA simultaneously and identifies diverse gene regulatory elements.Nature genetics · 2024Article
- Histone variant H2AZ1 drives lung cancer progression through the RELA-HIF1A-EGFR signaling pathway.Cell communication and signaling : CCS · 2024Article
- O-GlcNAc transferase congenital disorder of glycosylation (OGT-CDG): Potential mechanistic targets revealed by evaluating the OGT interactome.The Journal of biological chemistry · 2024Review
- Structural insights into the human NuA4/TIP60 acetyltransferase and chromatin remodeling complex.Science (New York, N.Y.) · 2024Article
- Notch signaling pathway in cancer: from mechanistic insights to targeted therapies.Signal transduction and targeted therapy · 2024Review
- Comprehensive genomic features indicative for Notch responsiveness.Nucleic acids research · 2024Article
- Control of Intestinal Stemness and Cell Lineage by Histone Variant H2A.Z Isoforms.Molecular and cellular biology · 2024Article
- Tip60-mediated H2A.Z acetylation promotes neuronal fate specification and bivalent gene activation.Molecular cell · 2022Article
- The structure, binding and function of a Notch transcription complex involving RBPJ and the epigenetic reader protein L3MBTL3.Nucleic acids research · 2022Article
- Notch-dependent and -independent functions of transcription factor RBPJ.Nucleic acids research · 2022Article
- Loss of TIP60 (KAT5) abolishes H2AZ lysine 7 acetylation and causes p53, INK4A, and ARF-independent cell cycle arrest.Cell death & disease · 2022Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A fundamental as yet incompletely understood feature of Notch signal transduction is a transcriptional shift from repression to activation that depends on chromatin regulation mediated by transcription factor RBP-J and associated cofactors. Incorporation of histone variants alter the functional properties of chromatin and are implicated in the regulation of gene expression. Here, we show that depletion of histone variant H2A.Z leads to upregulation of canonical Notch target genes and that the H2A.Z-chaperone TRRAP/p400/Tip60 complex physically associates with RBP-J at Notch-dependent enhancers. When targeted to RBP-J-bound enhancers, the acetyltransferase Tip60 acetylates H2A.Z and upregulates Notch target gene expression. Importantly, the Drosophila homologs of Tip60, p400 and H2A.Z modulate Notch signaling response and growth in vivo. Together, our data reveal that loading and acetylation of H2A.Z are required to assure tight control of canonical Notch activation.
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