ArticleMolecular cell2015
Histone Variant H2A.Z.2 Mediates Proliferation and Drug Sensitivity of Malignant Melanoma.
Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
134 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.
- Contribution of histone variants to aneuploidy: a cancer perspective.Frontiers in genetics · 2023Pooled it
- Downregulation of histone H2A and H2B pathways is associated with anthracycline sensitivity in breast cancer.Breast cancer research : BCR · 2016Trial
- ZNF512B associates with mitotic spindles, regulates metaphase exit, and is crucial for stem cell differentiation.Nucleic acids research · 2026Article
- Histone Variant H2A.Z2 Hyper-Transcription Induced by E2F1 Accelerates Lung Adenocarcinoma Progression via the JAK-STAT Signaling Pathway.Thoracic cancer · 2026Article
- Histone variant H2A.J is an epigenetic regulator of metastasis in lung adenocarcinoma.Cell death & disease · 2026Article
- mChIP-seq for Multiplex and Multifactorial Epigenomic Profiling Uncovers Cancer-specific Histone Features in Cellular and Circulating Nucleosomes.bioRxiv : the preprint server for biology · 2026Article
- PROTAC-based protein degradation: a window of opportunity for melanoma therapy.Journal of biomedical science · 2026Review
- Skin Epidermal Progenitor Maintenance by the SRCAP-H2A.Z Axis Downstream to Extracellular Signal-Regulated Kinase and mTOR Signaling.The Journal of investigative dermatology · 2026Article
- Cancer histone H2A.Z missense mutations disrupt function through distinct local and allosteric effects.Research square · 2026Article
- Melanoma: Pathogenesis and Targeted Therapy.MedComm · 2026Review
- The role of epigenetic modifications in hematological cancers.Frontiers in oncology · 2026Review
- SETDB1 is critically required for uveal melanoma growth and represents a promising therapeutic target.Cell death & disease · 2025Article
- BPTF Target Engagement by Acetylated H2A.Z Photoaffinity Probes.Biochemistry · 2025Article
- INO80/SWR remodelers regulate Pol II transcription through BRD2 and chromatin landscape.Nucleic acids research · 2025Article
- Article
- ANP32E drives vulnerability to ATR inhibitors by inducing R-loops-dependent transcription replication conflicts in triple negative breast cancer.Nature communications · 2025Article
- The SWI/SNF PBAF complex facilitates REST occupancy at repressive chromatin.Molecular cell · 2025Article
- Coupling Proximity Biotinylation with Genomic Targeting to Characterize Locus-Specific Changes in Chromatin Environments.Journal of proteome research · 2025Article
- The "Ins and Outs and What-Abouts" of H2A.Z: A tribute to C. David Allis.The Journal of biological chemistry · 2025Article
- Characterizing the regulatory effects of H2A.Z and SWR1-C on gene expression during hydroxyurea exposure in Saccharomyces cerevisiae.PLoS genetics · 2025Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 6 institutions in 3 countries.
Funding
Abstract
Histone variants are emerging as key regulatory molecules in cancer. We report a unique role for the H2A.Z isoform H2A.Z.2 as a driver of malignant melanoma. H2A.Z.2 is highly expressed in metastatic melanoma, correlates with decreased patient survival, and is required for cellular proliferation. Our integrated genomic analyses reveal that H2A.Z.2 controls the transcriptional output of E2F target genes in melanoma cells. These genes are highly expressed and display a distinct signature of H2A.Z occupancy. We identify BRD2 as an H2A.Z-interacting protein, levels of which are also elevated in melanoma. We further demonstrate that H2A.Z.2-regulated genes are bound by BRD2 and E2F1 in an H2A.Z.2-dependent manner. Importantly, H2A.Z.2 deficiency sensitizes melanoma cells to chemotherapy and targeted therapies. Collectively, our findings implicate H2A.Z.2 as a mediator of cell proliferation and drug sensitivity in malignant melanoma, holding translational potential for novel therapeutic strategies.
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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.