ArticleMolecular and cellular biology2013
Histone H3K27 trimethylation inhibits H3 binding and function of SET1-like H3K4 methyltransferase complexes.
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 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 69 citations in OpenAlex.
- O-GlcNAc transferase congenital disorder of glycosylation (OGT-CDG): Potential mechanistic targets revealed by evaluating the OGT interactome.The Journal of biological chemistry · 2024Review
- The COMPASS complex maintains the metastatic capacity imparted by a subpopulation of cells in UPS.iScience · 2024Article
- Nucleosomal asymmetry: a novel mechanism to regulate nucleosome function.Biochemical Society transactions · 2024Review
- The role of histone methyltransferases in neurocognitive disorders associated with brain size abnormalities.Frontiers in neuroscience · 2023Review
- KDM6A mutations promote acute cytoplasmic DNA release, DNA damage response and mitosis defects.BMC molecular and cell biology · 2021Article
- Non-canonical H3K79me2-dependent pathways promote the survival of MLL-rearranged leukemia.eLife · 2021Article
- The MLL3/4 H3K4 methyltransferase complex in establishing an active enhancer landscape.Biochemical Society transactions · 2021Review
- Aging mechanisms-A perspective mostly fromAdvanced genetics (Hoboken, N.J.) · 2020Article
- A Binary Arginine Methylation Switch on Histone H3 Arginine 2 Regulates Its Interaction with WDR5.Biochemistry · 2020Article
- KDM6A-Mediated Expression of the Long Noncoding RNA DINO Causes TP53 Tumor Suppressor Stabilization in Human Papillomavirus 16 E7-Expressing Cells.Journal of virology · 2020Article
- The transcription factor Nurr1 is upregulated in amyotrophic lateral sclerosis patients and SOD1-G93A mice.Disease models & mechanisms · 2020Article
- Chemoenzymatic Semisynthesis of Proteins.Chemical reviews · 2020Review
- Paradoxical Changes Underscore Epigenetic Reprogramming During Adult Zebrafish Extraocular Muscle Regeneration.Investigative ophthalmology & visual science · 2019Article
- PRC2 is high maintenance.Genes & development · 2019Review
- Theoretical analysis of Polycomb-Trithorax systems predicts that poised chromatin is bistable and not bivalent.Nature communications · 2019Article
- Article
- EMT is associated with an epigenetic signature of ECM remodeling genes.Cell death & disease · 2019Article
- Identification and functional characterization of Lys-trimethylation of lactate dehydrogenase A.OncoTargets and therapy · 2019Article
- Oral Delivery of miRNA With Lipidic Aminoglycoside Derivatives in the Breastfed Rat.Frontiers in physiology · 2019Article
- Cardiac-specific developmental and epigenetic functions of Jarid2 during embryonic development.The Journal of biological chemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Trimethylated histone H3 lysine 4 (H3K4) and H3K27 generally mark transcriptionally active and repressive chromatins, respectively. In most cell types, these two modifications are mutually exclusive, and this segregation is crucial for the regulation of gene expression. However, how this anticorrelation is achieved has not been fully understood. Here, we show that removal of the H3K27 trimethyl mark facilitates recruitment of SET1-like H3K4 methyltransferase complexes to their target genes by eliciting a novel interaction between histone H3 and two common subunits, WDR5 and RBBP5, of SET1-like complexes. Consistent with this result, H3K27 trimethylation destabilizes interactions of H3 with SET1-like complexes and antagonizes their ability to carry out H3K4 trimethylation of peptide (H3 residues 1 to 36), histone octamer, and mononucleosome substrates. Altogether, our studies reveal that H3K27 trimethylation of histone H3 represses a previously unrecognized interaction between H3 and SET1-like complexes. This provides an important mechanism that directs the anticorrelation between H3K4 and H3K27 trimethylation.
Indexed as
Identifiers
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.