ArticleThe Journal of biological chemistry2012
The atypical histone macroH2A1.2 interacts with HER-2 protein in cancer cells.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Regional Conservation and Transcriptional Regulation of Tumor-Associated Genes by macroH2A1 Deposition in Mammalian Cells.Biomolecules · 2025Article
- Roles of Histone H2A Variants in Cancer Development, Prognosis, and Treatment.International journal of molecular sciences · 2024Review
- CYB561 promotes HER2+ breast cancer proliferation by inhibiting H2AFY degradation.Cell death discovery · 2024Article
- Next-generation proteomics of serum extracellular vesicles combined with single-cell RNA sequencing identifies MACROH2A1 associated with refractory COVID-19.Inflammation and regeneration · 2022Article
- The Role of MacroH2A Histone Variants in Cancer.Cancers · 2021Review
- Article
- Prognostic and predictive value of a mRNA signature in peripheral T-cell lymphomas: A mRNA expression analysis.Journal of cellular and molecular medicine · 2021Article
- Exploring the Prognostic Value, Immune Implication and Biological Function ofFrontiers in immunology · 2021Article
- Canonical ErbB-2 isoform and ErbB-2 variant c located in the nucleus drive triple negative breast cancer growth.Oncogene · 2020Article
- MacroH2A1 Immunoexpression in Breast Cancer.Frontiers in oncology · 2020Article
- A three layered histone epigenetics in breast cancer metastasis.Cell & bioscience · 2020Review
- Zebrafish macroH2A variants have distinct embryo localization and function.Scientific reports · 2019Article
- Nuclear ErbB-2: a Novel Therapeutic Target in ErbB-2-Positive Breast Cancer?Hormones & cancer · 2019Review
- Analysis of HER2 genomic binding in breast cancer cells identifies a global role in direct gene regulation.PloS one · 2019Article
- Review
- Participation of GATA-3 in regulation of bone healing through transcriptional upregulation of bcl-xExperimental & molecular medicine · 2017Article
- Localisation Microscopy of Breast Epithelial ErbB-2 Receptors and Gap Junctions: Trafficking after γ-Irradiation, Neuregulin-1β, and Trastuzumab Application.International journal of molecular sciences · 2017Article
- QKI5-mediated alternative splicing of the histone variant macroH2A1 regulates gastric carcinogenesis.Oncotarget · 2016Article
- MacroH2A1 downregulation enhances the stem-like properties of bladder cancer cells by transactivation of Lin28B.Oncogene · 2016Article
- Proteolytic cleavage, trafficking, and functions of nuclear receptor tyrosine kinases.The FEBS journal · 2015Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Because HER-2 has been demonstrated in the nuclei of cancer cells, we hypothesized that it might interact with transcription factors that activate ERBB2 transcription. Macrohistone 2A1 (H2AFY; mH2A1) was found to interact with HER-2 in cancer cells that overexpress HER-2. Of the two human mH2A1 isoforms, mH2A1.2, but not mH2A1.1, interacted with HER-2 in human cancer cell lines. Overexpression of mH2A1.2, but not mH2A1.1, in cancer cells significantly increased HER-2 expression and tumorigenicity. Inhibition of HER-2 kinase activity diminished mH2A1 expression and mH2A1.2-induced ERBB2 transcription in cancer cells. Chromatin immunoprecipitation of mH2A1.2 in cancer cells stably transfected with mH2A1.2 showed enrichment of mH2A1.2 at the HER-2 promoter, suggesting a role for mH2A1.2 in driving HER-2 overexpression. The evolutionarily conserved macro domain of mH2A1.2 was sufficient for the interaction between HER-2 and mH2A1.2 and for mH2A1.2-induced ERBB2 transcription. Within the macro domain of mH2A1.2, a trinucleotide insertion (-EIS-) sequence not found in mH2A1.1 was essential for the interaction between HER-2 and mH2A1.2 as well as mH2A1.2-induced HER-2 expression and cell proliferation.
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Registered trials
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