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Cross-talk between Lysine-Modifying Enzymes Controls Site-Specific DNA Amplifications.
Mishra, Sweta; Van Rechem, Capucine; Pal, Sangita; Clarke, Thomas L; Chakraborty, Damayanti; Mahan, Sarah D; Black, Joshua C; Murphy, Sedona E; Lawrence, Michael S; Daniels, Danette L; Whetstine, Johnathan R.
Afiliación
  • Mishra S; Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
  • Van Rechem C; Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
  • Pal S; Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
  • Clarke TL; Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
  • Chakraborty D; Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
  • Mahan SD; Promega Corporation, 2800 Woods Hollow Road, Madison, WI 53711, USA.
  • Black JC; Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
  • Murphy SE; Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA.
  • Lawrence MS; Massachusetts General Hospital Cancer Center and Department of Pathology, Harvard Medical School, 13th Street, Charlestown, MA 02129, USA; Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, MA 02142, USA.
  • Daniels DL; Promega Corporation, 2800 Woods Hollow Road, Madison, WI 53711, USA.
  • Whetstine JR; Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, 13(th) Street, Charlestown, MA 02129, USA. Electronic address: jwhetstine@hms.harvard.edu.
Cell ; 174(4): 803-817.e16, 2018 08 09.
Article en En | MEDLINE | ID: mdl-30057114
Acquired chromosomal DNA amplifications are features of many tumors. Although overexpression and stabilization of the histone H3 lysine 9/36 (H3K9/36) tri-demethylase KDM4A generates transient site-specific copy number gains (TSSGs), additional mechanisms directly controlling site-specific DNA copy gains are not well defined. In this study, we uncover a collection of H3K4-modifying chromatin regulators that function with H3K9 and H3K36 regulators to orchestrate TSSGs. Specifically, the H3K4 tri-demethylase KDM5A and specific COMPASS/KMT2 H3K4 methyltransferases modulate different TSSG loci through H3K4 methylation states and KDM4A recruitment. Furthermore, a distinct chromatin modifier network, MLL1-KDM4B-KDM5B, controls copy number regulation at a specific genomic locus in a KDM4A-independent manner. These pathways comprise an epigenetic addressing system for defining site-specific DNA rereplication and amplifications.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Cromatina / Histonas / Metilación de ADN / Proteína 2 de Unión a Retinoblastoma / Variaciones en el Número de Copia de ADN / Lisina Límite: Humans Idioma: En Revista: Cell Año: 2018 Tipo del documento: Article País de afiliación: Estados Unidos
Texto completo
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Cromatina / Histonas / Metilación de ADN / Proteína 2 de Unión a Retinoblastoma / Variaciones en el Número de Copia de ADN / Lisina Límite: Humans Idioma: En Revista: Cell Año: 2018 Tipo del documento: Article País de afiliación: Estados Unidos