ArticleScientific reports2015
RE-IIBP Methylates H3K79 and Induces MEIS1-mediated Apoptosis via H2BK120 Ubiquitination by RNF20.
Article in Scientific reports, 2015. 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, 35 citations in OpenAlex.
- Loss of DOT1L disrupts neuronal transcription and leads to a neurodevelopmental disorder.Brain : a journal of neurology · 2026Article
- NSD Family-Mediated H3K36 Methylation in Human Cancer: Mechanisms and Therapeutic Opportunities.Biomedicines · 2025Review
- Loss of DOT1L disrupts neuronal transcription, behavior, and leads to a neurodevelopmental disorder.medRxiv : the preprint server for health sciences · 2025Article
- NSD family proteins: Rising stars as therapeutic targets.Cell insight · 2024Review
- Article
- The TUDOR domain of SMN is an H3K79Life science alliance · 2023Article
- The role of NSD1, NSD2, and NSD3 histone methyltransferases in solid tumors.Cellular and molecular life sciences : CMLS · 2022Review
- MLL5 is involved in retinal photoreceptor maturation through facilitating CRX-mediated photoreceptor gene transactivation.iScience · 2022Article
- Article
- Rnf20 deficiency in adipocyte impairs adipose tissue development and thermogenesis.Protein & cell · 2021Article
- The NSD2 p.E1099K Mutation Is Enriched at Relapse and Confers Drug Resistance in a Cell Context-Dependent Manner in Pediatric Acute Lymphoblastic Leukemia.Molecular cancer research : MCR · 2020Article
- LncRNA ODIR1 inhibits osteogenic differentiation of hUC-MSCs through the FBXO25/H2BK120ub/H3K4me3/OSX axis.Cell death & disease · 2019Article
- DOT1L promotes progenitor proliferation and primes neuronal layer identity in the developing cerebral cortex.Nucleic acids research · 2019Article
- Inhibitors of Protein Methyltransferases and Demethylases.Chemical reviews · 2018Review
- Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark.Journal of visualized experiments : JoVE · 2018Article
- Marked for death: targeting epigenetic changes in cancer.Nature reviews. Drug discovery · 2017Review
- MEIS1 inhibits clear cell renal cell carcinoma cells proliferation and in vitro invasion or migration.BMC cancer · 2017Article
- Tri-methylation of H3K79 is decreased in TGF-β1-induced epithelial-to-mesenchymal transition in lung cancer.Clinical epigenetics · 2017Article
- The upstreams and downstreams of H3K79 methylation by DOT1L.Chromosoma · 2016Review
- Optimization of a Fragment-Based Screening Hit toward Potent DOT1L Inhibitors Interacting in an Induced Binding Pocket.ACS medicinal chemistry letters · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone lysine methylation contributes to transcriptional regulation by serving as a platform for the recruitment of various cofactors. Intense studies have been conducted for elucidating the functional meaning of H3K79 methylation, and to date, the only known HMTase responsible for the modification was DOT1L. In this study, we report that the MMSET isoform RE-IIBP has HMTase activity for H3K79. It was uncovered that RE-IIBP up-regulates MEIS1 transcription through H3K79 methylation via recruitment to the MEIS1 promoter. By means of proteomic and biochemical analysis, association of RE-IIBP with the E3 ubiquitin ligase RNF20 was demonstrated for synergistic activation of MEIS1 transcription via H3K79 HMTase activity. Furthermore, It was observed that RE-IIBP induces MEIS1-mediated apoptosis, which was dependent on H2BK120 ubiquitination by RNF20. These findings suggest RE-IIBP as another candidate for further studies to elucidate the mechanism of H3K79 methylation and its biological functions.
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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.