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| http://dx.doi.org/10.1016/j.ccell.2019.01.012 | DOI Listing |
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The lysine-specific demethylase 5 (KDM5) family, a key post-translational modification of chromatin, can shape tumor immune microenvironment. Here, we performed an extensive clinical and bioinformatic analysis to explore the association between KDM5 mutation and tumor immunity and its impact on the outcomes in pan-cancer immunotherapy. In 2943 patients across 12 tumor types treated with immune checkpoint inhibitors, KDM5-mutant tumors were associated with favorable overall survival (hazard ratio, 0.
View Article and Find Full Text PDFKDM5 family proteins are best known for their demethylation of the promoter proximal chromatin mark H3K4me3. KDM5-regulated transcription is critical in the brain, with variants in the X-linked paralog causing the intellectual disability (ID) disorder Claes-Jensen syndrome. Although the demethylase activity of KDM5C is known to be important for neuronal function, the contribution of non-enzymatic activities remain less characterized.
View Article and Find Full Text PDFJmjC catalysed histone H2a N-methyl arginine demethylation and C4-arginine hydroxylation reveals importance of sequence-reactivity relationships.
Commun Biol
November 2024
Chemistry Research Laboratory, Department of Chemistry and the Ineos Oxford Institute for Antimicrobial Research, University of Oxford, Oxford, OX1 3TA, United Kingdom.
2-Oxoglutarate (2OG) dependent N-methyl lysine demethylases (JmjC-KDMs) regulate eukaryotic transcription. We report studies showing that isolated forms of all human KDM4 and KDM5 JmjC enzymes catalyse demethylation of N-methylated Arg-3 of histone H2a. Unexpectedly, the results reveal that KDM4E and, less efficiently, KDM4D catalyse C-4 hydroxylation of Arg-20 of H2a on peptides, recombinant H2a, and calf histone extracts, including when the Arg-20 guanidino group is N-methylated.
View Article and Find Full Text PDFZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer.
Cell Rep
December 2024
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; The Eli and Edythe L. Broad Institute, Cambridge, MA 02142, USA; Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA 02215, USA; The Ludwig Center at Harvard, Boston, MA 02115, USA. Electronic address:
Article Synopsis
- The study identifies KDM5A as an important oncogene in basal breast cancer, showing that its amplification and overexpression can be targeted to suppress cancer cell growth.
- CRISPR knockout screens reveal that deleting the ZBTB7A transcription factor makes cells more sensitive to KDM5 inhibition, while the deletion of RHO-GTPases provides resistance.
- The research highlights the role of ZBTB7A and KDM5A/B in regulating gene expression, particularly regarding NF-κB targets, and links high ZBTB7A levels to poorer treatment responses in triple-negative breast cancer.
Stat stimulates histone H3K4 methylation via KDM5 inhibition in adult stem cells of budding tunicates.
Dev Dyn
October 2024
Laboratory of Cellular and Molecular Biotechnology, Faculty of Science, Kochi University, Kochi, Japan.
Background: The branchial epithelium is one of the main tissues in which histone H3K4 trimethylation (H3K4me3) occurs in the budding tunicate, Polyandrocarpa misakiensis. It contains proliferating and undifferentiated cell aggregates at the bottom of each pharyngeal cleft, providing the nest for the adult stem cell niche. We examined the sustainable mechanism enabling epigenetic histone methylation in adult stem cells.
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