ArticleJournal of molecular biology2017
H3K4 Methyltransferase Activity Is Required for MLL4 Protein Stability.
Article in Journal of molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 59 citations in OpenAlex.
- The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers.Nature communications · 2026Article
- Targeting lysine-specific demethylase 1 inhibits melanoma metastasis via the NF2-Hippo-YAP pathway.Cell death & disease · 2026Article
- SLA2 is Associated With Immune evasion and Exhaustion of CD8Journal of cellular and molecular medicine · 2026Article
- Role of histone-lysine N-methyltransferase 2D (KMT2D) in MEK-ERK signaling-mediated epigenetic regulation: a phosphoproteomics perspective.Frontiers in bioinformatics · 2025Article
- Coding Variants of the Genitourinary Development GeneJCO precision oncology · 2025Article
- Growth deficiency in a mouse model of Kabuki syndrome 2 bears mechanistic similarities to Kabuki syndrome 1.PLoS genetics · 2024Article
- KMT2 Family of H3K4 Methyltransferases: Enzymatic Activity-dependent and -independent Functions.Journal of molecular biology · 2024Review
- Role of H3K4 monomethylation in gene regulation.Current opinion in genetics & development · 2024Review
- Functional Roles of H3K4 Methylation in Transcriptional Regulation.Molecular and cellular biology · 2024Review
- KMT2D preferentially binds mRNAs of the genes it regulates, suggesting a role in RNA processing.Protein science : a publication of the Protein Society · 2024Article
- Somatic mutations of MLL4/COMPASS induce cytoplasmic localization providing molecular insight into cancer prognosis and treatment.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Leveraging dominant-negative histone H3 K-to-M mutations to study chromatin during differentiation and development.Development (Cambridge, England) · 2023Review
- Loss of Histone Methyltransferase KMT2D Attenuates Angiogenesis in the Ischemic Heart by Inhibiting the Transcriptional Activation of VEGF-A.Journal of cardiovascular translational research · 2023Article
- Epigenetic moonlighting: Catalytic-independent functions of histone modifiers in regulating transcription.Science advances · 2023Review
- Sexual dimorphism in bladder cancer: a review of etiology, biology, diagnosis, and outcomes.Frontiers in pharmacology · 2023Review
- Characterization of sequence determinants of enhancer function using natural genetic variation.eLife · 2022Article
- M2-like tumor-associated macrophages transmit exosomal miR-27b-3p and maintain glioblastoma stem-like cell properties.Cell death discovery · 2022Article
- Mechanism of Sex Differences in Bladder Cancer: Evident and Elusive Sex-biasing Factors.Bladder cancer (Amsterdam, Netherlands) · 2022Review
- The low-complexity domains of the KMT2D protein regulate histone monomethylation transcription to facilitate pancreatic cancer progression.Cellular & molecular biology letters · 2021Article
- Lysine methyltransferase 2D regulates muscle fiber size and muscle cell differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Transcriptional enhancers play a key role in cell type-specific gene expression and cell fate transition. Enhancers are marked by histone H3K4 mono- and di-methylation (H3K4me1/2). The tumor suppressor MLL4 (KMT2D) is a major enhancer H3K4 mono- and di-methyltransferase with a partial functional redundancy with MLL3 (KMT2C). However, the functional role of MLL4 enzymatic activity remains elusive. To address this issue, we have generated MLL4 enzyme-dead knock-in (KI) embryonic stem (ES) cells and mice, which carry Y5477A/Y5523A/Y5563A mutations in the enzymatic SET domain of the MLL4 protein. Homozygous MLL4 enzyme-dead KI (Mll4
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What OpenQuestion holds
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.