ArticleOncogene2013
H2A.Z-dependent crosstalk between enhancer and promoter regulates cyclin D1 expression.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 49 citations in OpenAlex.
- H2A.Z is essential for oocyte maturation and fertility in female mouse.Nature structural & molecular biology · 2025Article
- Structural insights into the human NuA4/TIP60 acetyltransferase and chromatin remodeling complex.Science (New York, N.Y.) · 2024Article
- Nucleosome Dynamics Derived at the Single-Molecule Level Bridges Its Structures and Functions.JACS Au · 2024Review
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- TIP60 is required for tumorigenesis in non-small cell lung cancer.Cancer science · 2023Article
- H3K4me1 Modification Functions in Caste Differentiation in Honey Bees.International journal of molecular sciences · 2023Article
- Tip60-mediated H2A.Z acetylation promotes neuronal fate specification and bivalent gene activation.Molecular cell · 2022Article
- Loss of TIP60 (KAT5) abolishes H2AZ lysine 7 acetylation and causes p53, INK4A, and ARF-independent cell cycle arrest.Cell death & disease · 2022Article
- Non-canonical roles of canonical telomere binding proteins in cancers.Cellular and molecular life sciences : CMLS · 2021Review
- Solid tumours hijack the histone variant network.Nature reviews. Cancer · 2021Review
- Article
- DNA repair complex licenses acetylation of H2A.Z.1 by KAT2A during transcription.Nature chemical biology · 2019Article
- The histone variant H2A.Z and chromatin remodeler BRAHMA act coordinately and antagonistically to regulate transcription and nucleosome dynamics in Arabidopsis.The Plant journal : for cell and molecular biology · 2019Article
- The histone variant H2A.Z in gene regulation.Epigenetics & chromatin · 2019Review
- The H2A.Z histone variant integrates Wnt signaling in intestinal epithelial homeostasis.Nature communications · 2019Article
- Nasal DNA methylation is associated with childhood asthma.Epigenomics · 2018Article
- Brain-specific deletion of histone variant H2A.z results in cortical neurogenesis defects and neurodevelopmental disorder.Nucleic acids research · 2018Article
- SUMO modification system facilitates the exchange of histone variant H2A.Z-2 at DNA damage sites.Nucleus (Austin, Tex.) · 2018Article
- Acetylated histone variant H2A.Z is involved in the activation of neo-enhancers in prostate cancer.Nature communications · 2017Article
- The Role of Pontin and Reptin in Cellular Physiology and Cancer Etiology.Frontiers in molecular biosciences · 2017Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
H2A.Z association with specific genomic loci is thought to contribute to a chromatin structure that promotes transcription activation. Acetylation of H2A.Z at promoters of oncogenes has been linked to tumorigenesis. The mechanism is unknown. Here, we show that in triple negative breast cancer cells, H2A.Z bound to the promoter of the constitutively, weakly expressed cyclin D1 oncogene (CCND1), a key regulator of cellular proliferation. Depleting the pool of H2A.Z stimulated transcription of CCND1 in the absence of its cognate transcription factor, the estrogen receptor (ER). During activation of CCND1, H2A.Z was released from the transcription start site (TSS) and downstream enhancer (enh2) sequences. Concurrently, acetylation of H2A.Z, H3 and H4 at the TSS was increased but only H2A.Z was acetylated at enh2. Acetylation of H2A.Z required the Tip60 acetyltransferase to be associated with the activated CCND1 on both TSS and enh2 sites. Depletion of Tip60 prevented CCND1 activation. Chromosome conformation capture experiments (3C) revealed specific contacts between the TSS and enh2 chromatin regions. These results suggest that release of a histone H2A.Z-mediated repression loop activates CCND1 for transcription. Our findings open new avenues for controlling and understanding aberrant gene expression associated with tumorigenesis.
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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.