ArticleNature cell biology2025
A SETD2-CDK1-lamin axis maintains nuclear morphology and genome stability.
Article in Nature cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Proteomic analysis of cisplatin-induced spermatogenesis defects in mice.Annals of medicine · 2026Article
- SETD2 Improves Endothelial Function and Angiogenesis in Diabetic Hindlimb Ischemia Via Activating ANGPT2-PI3K/AKT Pathway.Cardiovascular toxicology · 2026Article
- Deciphering mitotic catastrophe-associated transcriptomic patterns in renal cell carcinoma: prognostic significance and immunotherapy-related associations.Biology direct · 2026Article
- Getting nuclear size just right - emerging mechanisms regulating nuclear scaling and morphology.Journal of cell science · 2026Review
- MLL3/4 methyltransferases regulate the differentiation of pluripotent stem cells through coordinating glycolysis and mitochondrial respiration.bioRxiv : the preprint server for biology · 2026Article
- Article
- Baculoviruses exploit the mitotic kinase CDK1 to disrupt the nuclear lamina.PLoS pathogens · 2026Article
- Chromosome 3p deletion leads to extensive genomic alterations in diverse cancers and confers synthetic lethality in uveal melanoma.bioRxiv : the preprint server for biology · 2026Article
- Forceful Beginnings: Mechanotransduction and Mechanosensation at the Meiotic Cell Nucleus During Gamete Development.Results and problems in cell differentiation · 2026Review
- Loss of SETD2-mediated H3K36me3 Drives CD8Research (Washington, D.C.) · 2026Article
- Nickel Nanoparticles Promote Lung Adenocarcinoma Progression via CDK1-Mediated Fatty Acid Metabolism Regulation.International journal of molecular sciences · 2025Article
- Molecular mechanism of co-transcriptional H3K36 methylation by SETD2.Nature communications · 2025Article
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Authors and funding
19 authors.
Funding
Abstract
Histone methyltransferases regulate chromatin organization and are frequently mutated in human diseases, including cancer. One such often mutated methyltransferase, SETD2, associates with transcribing RNA polymerase II and catalyses H3K36me3-a modification that contributes to gene transcription, splicing and DNA repair. Although its catalytic function is well-characterized, its non-catalytic roles remain unclear. Here we reveal a catalysis-independent function of SETD2 in nuclear lamina stability and genome integrity. Through its intrinsically disordered amino terminus, SETD2 associates with lamina-associated proteins, including lamin A/C, lamin B1 and emerin. Loss of SETD2 or its N terminus leads to severe nuclear morphology defects and genome instability, mirroring lamina dysfunction. Mechanistically, the N terminus of SETD2 serves as a scaffold for the mitotic kinase CDK1 and lamins, facilitating lamin phosphorylation and depolymerization during mitosis. Restoration of the N-terminal regions required for interaction with CDK1 and lamins rescues nuclear morphology and suppresses tumorigenic growth in a clear cell renal cell carcinoma model with SETD2 haploinsufficiency. These findings reveal a previously unrecognized role of SETD2 in nuclear lamina organization and genome maintenance that probably extends to its role as a tumour suppressor.
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