ReviewCellular and molecular life sciences : CMLS2019
Why are so many MLL lysine methyltransferases required for normal mammalian development?
Review in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
- Targeting the Menin-KMT2A interaction in leukemia: Lessons learned and future directions.International journal of cancer · 2026Review
- Remembering foods and foes: emerging principles of transcriptional memory.Cell death and differentiation · 2025Review
- Binding to the Other Side: The AT-Hook DNA-Binding Domain Allows Nuclear Factors to Exploit the DNA Minor Groove.International journal of molecular sciences · 2024Review
- H3K4me1 facilitates promoter-enhancer interactions and gene activation during embryonic stem cell differentiation.Molecular cell · 2024Article
- Molecular complexity of diffuse large B-cell lymphoma: a molecular perspective and therapeutic implications.Journal of applied genetics · 2024Review
- In vivo screening characterizes chromatin factor functions during normal and malignant hematopoiesis.Nature genetics · 2023Article
- MLL methyltransferases regulate H3K4 methylation to ensure CENP-A assembly at human centromeres.PLoS biology · 2023Article
- Deep computational phenotyping of genomic variants impacting the SET domain of KMT2C reveal molecular mechanisms for their dysfunction.Frontiers in genetics · 2023Article
- Mutations in epigenetic regulatorOncology research · 2023Article
- ASXL1/2 mutations and myeloid malignancies.Journal of hematology & oncology · 2022Review
- Differences in H3K4me3 and chromatin accessibility contribute to altered T-cell receptor signaling in neonatal naïve CD4 T cells.Immunology and cell biology · 2022Article
- Lysine methyltransferase inhibitors: where we are now.RSC chemical biology · 2022Review
- Essential Functions of MLL1 and MLL2 in Retinal Development and Cone Cell Maintenance.Frontiers in cell and developmental biology · 2022Article
- Structure, Activity and Function of the MLL2 (KMT2B) Protein Lysine Methyltransferase.Life (Basel, Switzerland) · 2021Review
- Review
- Setd1a Plays Pivotal Roles for the Survival and Proliferation of Retinal Progenitors via Histone Modifications of Uhrf1.Investigative ophthalmology & visual science · 2021Article
- Allosteric regulation of histone lysine methyltransferases: from context-specific regulation to selective drugs.Biochemical Society transactions · 2021Review
- Epigenetic Control of Infant B Cell Precursor Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2021Review
- The Role of H3K4 Trimethylation in CpG Islands Hypermethylation in Cancer.Biomolecules · 2021Review
- SETD1A Mediated H3K4 Methylation and Its Role in Neurodevelopmental and Neuropsychiatric Disorders.Frontiers in molecular neuroscience · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The mixed lineage leukemia (MLL) family of proteins became known initially for the leukemia link of its founding member. Over the decades, the MLL family has been recognized as an important class of histone H3 lysine 4 (H3K4) methyltransferases that control key aspects of normal cell physiology and development. Here, we provide a brief history of the discovery and study of this family of proteins. We address two main questions: why are there so many H3K4 methyltransferases in mammals; and is H3K4 methylation their key function?
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Registered trials
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.