ReviewCellular and molecular life sciences : CMLS2022
SETD2: from chromatin modifier to multipronged regulator of the genome and beyond.
Review in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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
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Who cites it
34 citing papers in PubMed, 50 citations in OpenAlex.
- SETD2 is a novel and druggable dependency in IMiD/CELMoD resistant multiple myeloma models.Blood cancer journal · 2026Article
- Article
- Regulation of the histone H3K36 methyltransferase Set2 by the histone chaperone Spt6.Nucleic acids research · 2026Article
- AURORA A interacts with DICER and SETD2 to promote S-phase progression.EMBO reports · 2026Article
- SETD2 Improves Endothelial Function and Angiogenesis in Diabetic Hindlimb Ischemia Via Activating ANGPT2-PI3K/AKT Pathway.Cardiovascular toxicology · 2026Article
- Regulation of the histone H3K36 methyltransferase Set2 by the histone chaperone Spt6.bioRxiv : the preprint server for biology · 2026Article
- CLOCK-catalyzed histone H3K37 glutarylation suppresses H3K36 trimethylation pathways in glioblastoma.Science advances · 2026Article
- Article
- SETD2 inhibited T-cell acute lymphocytic leukemia invasion and infiltration by inhibiting the JAK/STAT pathway.Molecular and cellular biochemistry · 2026Article
- The SETD2 L1609P mutation found in leukemia disrupts methyltransferase activity and reduces histone H3K36 trimethylation.The Journal of biological chemistry · 2026Article
- Structural basis of transcription-coupled H3K36 trimethylation by Set2 in coordination with FACT.Science advances · 2026Article
- Histone methyltransferase G9a crosstalks with H3K36 histone methyltransferases NSD3 and SETD2 to mediate gene activation.Frontiers in cell and developmental biology · 2026Article
- DNA methylation landscapes in human cells and their chromatin determinants.Ageing and cancer research & treatment · 2026Article
- Characterizing the Clinical and Molecular Profile of SETD2-Mutated Lung Adenocarcinoma.Cancers · 2025Article
- Emerging role of SETD2 in the development and function of immune cells.Genes & diseases · 2025Review
- Molecular mechanism of co-transcriptional H3K36 methylation by SETD2.Nature communications · 2025Article
- Transcriptional stochasticity reveals multiple mechanisms of long non-coding RNA regulation at the Xist-Tsix locus.Nature communications · 2025Article
- Review
- Genomic context-dependent histone H3K36 methylation by three Drosophila methyltransferases and implications for dedicated chromatin readers.Nucleic acids research · 2025Article
- Chromatin modifiers in neurodevelopment.Frontiers in molecular neuroscience · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Histone modifying enzymes play critical roles in many key cellular processes and are appealing proteins for targeting by small molecules in disease. However, while the functions of histone modifying enzymes are often linked to epigenetic regulation of the genome, an emerging theme is that these enzymes often also act by non-catalytic and/or non-epigenetic mechanisms. SETD2 (Set2 in yeast) is best known for associating with the transcription machinery and methylating histone H3 on lysine 36 (H3K36) during transcription. This well-characterized molecular function of SETD2 plays a role in fine-tuning transcription, maintaining chromatin integrity, and mRNA processing. Here we give an overview of the various molecular functions and mechanisms of regulation of H3K36 methylation by Set2/SETD2. These fundamental insights are important to understand SETD2's role in disease, most notably in cancer in which SETD2 is frequently inactivated. SETD2 also methylates non-histone substrates such as α-tubulin which may promote genome stability and contribute to the tumor-suppressor function of SETD2. Thus, to understand its role in disease, it is important to understand and dissect the multiple roles of SETD2 within the cell. In this review we discuss how histone methylation by Set2/SETD2 has led the way in connecting histone modifications in active regions of the genome to chromatin functions and how SETD2 is leading the way to showing that we also have to look beyond histones to truly understand the physiological role of an 'epigenetic' writer enzyme in normal cells and in disease.
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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.