ArticleNucleic acids research2014
The PR-Set7 binding domain of Riz1 is required for the H4K20me1-H3K9me1 trans-tail 'histone code' and Riz1 tumor suppressor function.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.Biomarker research · 2026Review
- The downregulation of RIZ1 activates the AKT/mTOR in pregnant women with obesity.Scientific reports · 2025Article
- Multiple functions of the lysine methyltransferase KMT5a in cancer: potential targets for innovative therapies.Clinical epigenetics · 2025Review
- PRDM2-The Key Research Targets for the Development of Diseases in Various Systems.Biomolecules · 2025Review
- Epigenetic Dysregulation in Alcohol-Associated Behaviors: Preclinical and Clinical Evidence.Current topics in behavioral neurosciences · 2025Review
- Distinct developmental phenotypes result from mutation of Set8/KMT5A and histone H4 lysine 20 in Drosophila melanogaster.Genetics · 2022Article
- Multifaceted Role of PRDM Proteins in Human Cancer.International journal of molecular sciences · 2020Review
- Utility of histone H3K27me3 and H4K20me as diagnostic indicators of melanoma.Melanoma research · 2020Article
- The histone methyltransferase Setd8 alters the chromatin landscape and regulates the expression of key transcription factors during erythroid differentiation.Epigenetics & chromatin · 2020Article
- Monomethyltransferase SET8 facilitates hepatocellular carcinoma growth by enhancing aerobic glycolysis.Cell death & disease · 2019Article
- Repression of Akt3 gene transcription by the tumor suppressor RIZ1.Scientific reports · 2018Article
- Dependence-induced increase of alcohol self-administration and compulsive drinking mediated by the histone methyltransferase PRDM2.Molecular psychiatry · 2017Article
- SomaticOncotarget · 2017Article
- Targeting histone methylation for colorectal cancer.Therapeutic advances in gastroenterology · 2017Review
- Synergism between RIZ1 gene therapy and paclitaxel in SiHa cervical cancer cells.Cancer gene therapy · 2016Article
- Methylation of histone H4 lysine 20 by PR-Set7 ensures the integrity of late replicating sequence domains in Drosophila.Nucleic acids research · 2016Article
- A fine balance: epigenetic control of cellular quiescence by the tumor suppressor PRDM2/RIZ at a bivalent domain in the cyclin a gene.Nucleic acids research · 2015Article
- Lower PRDM2 expression is associated with dopamine-agonist resistance and tumor recurrence in prolactinomas.BMC cancer · 2015Article
- Histone methyltransferases: novel targets for tumor and developmental defects.American journal of translational research · 2015Review
- The emerging role of lysine methyltransferase SETD8 in human diseases.Clinical epigeneticsReview
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
PR-Set7/Set8/KMT5a is the sole histone H4 lysine 20 monomethyltransferase (H4K20me1) in metazoans and is essential for proper cell division and genomic stability. We unexpectedly discovered that normal cellular levels of monomethylated histone H3 lysine 9 (H3K9me1) were also dependent on PR-Set7, but independent of its catalytic activity. This observation suggested that PR-Set7 interacts with an H3K9 monomethyltransferase to establish the previously reported H4K20me1-H3K9me1 trans-tail 'histone code'. Here we show that PR-Set7 specifically and directly binds the C-terminus of the Riz1/PRDM2/KMT8 tumor suppressor and demonstrate that the N-terminal PR/SET domain of Riz1 preferentially monomethylates H3K9. The PR-Set7 binding domain was required for Riz1 nuclear localization and maintenance of the H4K20me1-H3K9me1 trans-tail 'histone code'. Although Riz1 can function as a repressor, Riz1/H3K9me1 was dispensable for the repression of genes regulated by PR-Set7/H4K20me1. Frameshift mutations resulting in a truncated Riz1 incapable of binding PR-Set7 occur frequently in various aggressive cancers. In these cancer cells, expression of wild-type Riz1 restored tumor suppression by decreasing proliferation and increasing apoptosis. These phenotypes were not observed in cells expressing either the Riz1 PR/SET domain or PR-Set7 binding domain indicating that Riz1 methyltransferase activity and PR-Set7 binding domain are both essential for Riz1 tumor suppressor function.
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