ArticleMolecular and cellular biology2013
The histone methyltransferase KMT2B is required for RNA polymerase II association and protection from DNA methylation at the MagohB CpG island promoter.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Somatic mutations in angiogenesis-related pathways and RNA polymerase II activity in sporadic brain arteriovenous malformations.Frontiers in neurology · 2025Article
- An Updated Review on the Significance of DNA and Protein Methyltransferases and De-methylases in Human Diseases: From Molecular Mechanism to Novel Therapeutic Approaches.Current medicinal chemistry · 2024Review
- Phase I study of LZM005 in patients with HER2-positive metastatic breast cancer.NPJ breast cancer · 2022Article
- Repression of germline genes by PRC1.6 and SETDB1 in the early embryo precedes DNA methylation-mediated silencing.Nature communications · 2021Article
- MLL1 is required for maintenance of intestinal stem cells.PLoS genetics · 2021Article
- Structure, Activity and Function of the MLL2 (KMT2B) Protein Lysine Methyltransferase.Life (Basel, Switzerland) · 2021Review
- SET1/MLL family of proteins: functions beyond histone methylation.Epigenetics · 2021Review
- The MLL/SET family and haematopoiesis.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020Review
- The Mitochondrial Protein VDAC1 at the Crossroads of Cancer Cell Metabolism: The Epigenetic Link.Cancers · 2020Article
- MAGOH/MAGOHB Inhibits the Tumorigenesis of Gastric Cancer via Inactivation of b-RAF/MEK/ERK Signaling.OncoTargets and therapy · 2020Article
- One-Carbon Metabolism Links Nutrition Intake to Embryonic Development via Epigenetic Mechanisms.Stem cells international · 2019Review
- Promoter bivalency favors an open chromatin architecture in embryonic stem cells.Nature genetics · 2018Article
- Modes of Interaction of KMT2 Histone H3 Lysine 4 Methyltransferase/COMPASS Complexes with Chromatin.Cells · 2018Review
- MLL2, Not MLL1, Plays a Major Role in Sustaining MLL-Rearranged Acute Myeloid Leukemia.Cancer cell · 2017Article
- Neuronal Deletion of Kmt2a/Mll1 Histone Methyltransferase in Ventral Striatum is Associated with Defective Spike-Timing-Dependent Striatal Synaptic Plasticity, Altered Response to Dopaminergic Drugs, and Increased Anxiety.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Deciphering the Epigenetic Code in Embryonic and Dental Pulp Stem Cells.The Yale journal of biology and medicine · 2016Review
- MLL2 is essential for porcine embryo development in vitro.In vitro cellular & developmental biology. Animal · 2016Article
- Detection of uracil within DNA using a sensitive labeling method for in vitro and cellular applications.Nucleic acids research · 2016Article
- Neuronal Kmt2a/Mll1 histone methyltransferase is essential for prefrontal synaptic plasticity and working memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Molecular Profiling of a Rare Rosette-Forming Glioneuronal Tumor Arising in the Spinal Cord.PloS one · 2015Article
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
KMT2B (MLL2/WBP7) is a member of the MLL subfamily of H3K4-specific histone lysine methyltransferases (KMT2) and is vital for normal embryonic development in the mouse. To gain insight into the molecular mechanism underlying KMT2B function, we focused on MagohB, which is controlled by a CpG island promoter. We show that in cells lacking Mll2-the gene encoding KMT2B-the MagohB promoter resides in inaccessible chromatin and is methylated. To dissect the molecular events leading to the establishment of silencing, we performed kinetic studies in Mll2-conditional-knockout embryonic stem cells. KMT2B depletion was followed by the loss of the active chromatin marks and progressive loss of RNA polymerase II binding with a concomitant downregulation of MagohB expression. Once the active chromatin marks were lost, the MagohB promoter was rapidly methylated. We demonstrate that in the presence of KMT2B, neither transcription elongation nor RNA polymerase II binding is required to maintain H3K4 trimethylation at the MagohB promoter and protect it from DNA methylation. Reexpression of KMT2B was sufficient to reinstate an active MagohB promoter. Our study provides a paradigm for the idea that KMT2 proteins are crucial components for establishing and maintaining the transcriptionally active and unmethylated state of CpG island promoters.
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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.