ArticleThe Journal of biological chemistry2008
Dominant alleles identify SET domain residues required for histone methyltransferase of Polycomb repressive complex 2.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 52 citations in OpenAlex.
- A mouse model of Weaver syndrome displays overgrowth and excess osteogenesis reversible with KDM6A/6B inhibition.JCI insight · 2024Article
- LncRNA MYLK-AS1 acts as an oncogene by epigenetically silencing large tumor suppressor 2 (LATS2) in gastric cancer.Bioengineered · 2021Article
- Treating lymphoma is now a bit EZ-er.Blood advances · 2021Review
- The Pivotal Immunomodulatory and Anti-Inflammatory Effect of Histone-Lysine N-Methyltransferase in the Glioma Microenvironment: Its Biomarker and Therapy Potentials.Analytical cellular pathology (Amsterdam) · 2021Review
- Long noncoding RNA HOXA-AS2 functions as an oncogene by binding to EZH2 and suppressing LATS2 in acute myeloid leukemia (AML).Cell death & disease · 2020Article
- Identification and Functional Characterization of a New Splicing Variant of EZH2 in the Central Nervous System.International journal of biological sciences · 2019Article
- Article
- Long noncoding RNA MEG3 regulates LATS2 by promoting the ubiquitination of EZH2 and inhibits proliferation and invasion in gallbladder cancer.Cell death & disease · 2018Article
- Ezh2 promotes clock function and hematopoiesis independent of histone methyltransferase activity in zebrafish.Nucleic acids research · 2018Article
- Article
- Inhibitors of Protein Methyltransferases and Demethylases.Chemical reviews · 2018Review
- Polycomb Repressive Complex 2 Methylates Elongin A to Regulate Transcription.Molecular cell · 2017Article
- Article
- EZH2 in Cancer Progression and Potential Application in Cancer Therapy: A Friend or Foe?International journal of molecular sciences · 2017Review
- Chronic Myelogenous Leukemia- Initiating Cells Require Polycomb Group Protein EZH2.Cancer discovery · 2016Article
- Weaver Syndrome-Associated EZH2 Protein Variants Show Impaired Histone Methyltransferase Function In Vitro.Human mutation · 2016Article
- Adaptive selection and coevolution at the proteins of the Polycomb repressive complexes in Drosophila.Heredity · 2016Article
- Regulation and role of post-translational modifications of enhancer of zeste homologue 2 in cancer development.American journal of cancer research · 2016Review
- Role of bacterial infection in the epigenetic regulation of Wnt antagonist WIF1 by PRC2 protein EZH2.Oncogene · 2015Article
- Selective inhibitors of protein methyltransferases.Journal of medicinal chemistry · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycomb gene silencing requires histone methyltransferase activity of Polycomb repressive complex 2 (PRC2), which methylates lysine 27 of histone H3. Information on how PRC2 works is limited by lack of structural data on the catalytic subunit, Enhancer of zeste (E(Z)), and the paucity of E(z) mutant alleles that alter its SET domain. Here we analyze missense alleles of Drosophila E(z), selected for molecular study because of their dominant genetic effects. Four missense alleles identify key E(Z) SET domain residues, and a fifth is located in the adjacent CXC domain. Analysis of mutant PRC2 complexes in vitro, and H3-K27 methylation in vivo, shows that each SET domain mutation disrupts PRC2 histone methyltransferase. Based on known SET domain structures, the mutations likely affect either the lysine-substrate binding pocket, the binding site for the adenosylmethionine methyl donor, or a critical tyrosine predicted to interact with the substrate lysine epsilon-amino group. In contrast, the CXC mutant retains catalytic activity, Lys-27 specificity, and trimethylation capacity. Deletion analysis also reveals a functional requirement for a conserved E(Z) domain N-terminal to CXC and SET. These results identify critical SET domain residues needed for PRC2 enzyme function, and they also emphasize functional inputs from outside the SET domain.
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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.