Loss of BAP1 function leads to EZH2-dependent transformation

[1]  Tim J. Wigle,et al.  EPZ011989, A Potent, Orally-Available EZH2 Inhibitor with Robust in Vivo Activity , 2015, ACS medicinal chemistry letters.

[2]  W. Huber,et al.  Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2 , 2014, Genome Biology.

[3]  J. O’Shea,et al.  Faculty Opinions recommendation of Immunogenetics. Chromatin state dynamics during blood formation. , 2014 .

[4]  N. Friedman,et al.  Chromatin state dynamics during blood formation , 2014, Science.

[5]  David Shum,et al.  Small-Molecule Inhibitors of SETD8 with Cellular Activity , 2014, ACS chemical biology.

[6]  K. Coombes,et al.  Expression profiling stratifies mesothelioma tumors and signifies deregulation of spindle checkpoint pathway and microtubule network with therapeutic implications. , 2014, Annals of oncology : official journal of the European Society for Medical Oncology.

[7]  C. Mason,et al.  Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo , 2013, The Journal of experimental medicine.

[8]  O. Elemento,et al.  EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation. , 2013, Cancer cell.

[9]  Tim J. Wigle,et al.  Durable tumor regression in genetically altered malignant rhabdoid tumors by inhibition of methyltransferase EZH2 , 2013, Proceedings of the National Academy of Sciences.

[10]  Heng Li.  Aligning sequence reads, clone sequences and assembly contigs with BWA-MEM , 2013, 1303.3997.

[11]  V. Marquez,et al.  Inhibition of EZH2 suppresses self-renewal and induces radiation sensitivity in atypical rhabdoid teratoid tumor cells. , 2013, Neuro-oncology.

[12]  Yan Liu,et al.  EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations , 2012, Nature.

[13]  Somasekar Seshagiri,et al.  Loss of the Tumor Suppressor BAP1 Causes Myeloid Transformation , 2012, Science.

[14]  R. Young,et al.  The polycomb group protein L3mbtl2 assembles an atypical PRC1-family complex that is essential in pluripotent stem cells and early development. , 2012, Cell stem cell.

[15]  Iannis Aifantis,et al.  ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression. , 2012, Cancer cell.

[16]  N. Grishin,et al.  BAP1 loss defines a new class of renal cell carcinoma , 2012, Nature Genetics.

[17]  Steven L Salzberg,et al.  Fast gapped-read alignment with Bowtie 2 , 2012, Nature Methods.

[18]  Mitchell Ho,et al.  Rapid Generation of In Vitro Multicellular Spheroids for the Study of Monoclonal Antibody Therapy , 2011, Journal of Cancer.

[19]  Steven J. M. Jones,et al.  Frequent mutation of histone modifying genes in non-Hodgkin lymphoma , 2011, Nature.

[20]  Raul Rabadan,et al.  Analysis of the Coding Genome of Diffuse Large B-Cell Lymphoma , 2011, Nature Genetics.

[21]  C. Sander,et al.  The nuclear deubiquitinase BAP1 is commonly inactivated by somatic mutations and 3p21.1 losses in malignant pleural mesothelioma , 2011, Nature Genetics.

[22]  D. Neuberg,et al.  Clinical effect of point mutations in myelodysplastic syndromes. , 2011, The New England journal of medicine.

[23]  J. Harrow,et al.  A conditional knockout resource for the genome-wide study of mouse gene function , 2011, Nature.

[24]  D. Reinberg,et al.  L3MBTL2 protein acts in concert with PcG protein-mediated monoubiquitination of H2A to establish a repressive chromatin structure. , 2011, Molecular cell.

[25]  D. Gilliland,et al.  Concomitant analysis of EZH2 and ASXL1 mutations in myelofibrosis, chronic myelomonocytic leukemia and blast-phase myeloproliferative neoplasms , 2010, Leukemia.

[26]  P. Farnham,et al.  Using ChIP-seq technology to generate high-resolution profiles of histone modifications. , 2011, Methods in molecular biology.

[27]  A. Bowcock,et al.  Frequent Mutation of BAP1 in Metastasizing Uveal Melanomas , 2010, Science.

[28]  Scott L Pomeroy,et al.  Epigenetic antagonism between polycomb and SWI/SNF complexes during oncogenic transformation. , 2010, Cancer cell.

[29]  S. Akbarian,et al.  Chromatin Protein L3MBTL1 Is Dispensable for Development and Tumor Suppression in Mice* , 2010, The Journal of Biological Chemistry.

[30]  C. Glass,et al.  Simple combinations of lineage-determining transcription factors prime cis-regulatory elements required for macrophage and B cell identities. , 2010, Molecular cell.

[31]  M. Wilm,et al.  Histone H2A deubiquitinase activity of the Polycomb repressive complex PR-DUB , 2010, Nature.

[32]  Brendan MacLean,et al.  Bioinformatics Applications Note Gene Expression Skyline: an Open Source Document Editor for Creating and Analyzing Targeted Proteomics Experiments , 2022 .

[33]  Aaron R. Quinlan,et al.  BIOINFORMATICS APPLICATIONS NOTE , 2022 .

[34]  Daniel Birnbaum,et al.  Mutations of polycomb‐associated gene ASXL1 in myelodysplastic syndromes and chronic myelomonocytic leukaemia , 2009, British journal of haematology.

[35]  Randy J. Read,et al.  Methylation-state-specific recognition of histones by the MBT repeat protein L3MBTL2 , 2009, Nucleic acids research.

[36]  Xiaobo Xia,et al.  H3K79 methylation profiles define murine and human MLL-AF4 leukemias. , 2008, Cancer cell.

[37]  D. Reinberg,et al.  L3MBTL1, a Histone-Methylation-Dependent Chromatin Lock , 2007, Cell.

[38]  Scott A. Busby,et al.  Chemical derivatization of histones for facilitated analysis by mass spectrometry , 2007, Nature Protocols.

[39]  B. Chait,et al.  Ezh2 controls B cell development through histone H3 methylation and Igh rearrangement , 2003, Nature Immunology.

[40]  Paul Tempst,et al.  PR-Set7 is a nucleosome-specific methyltransferase that modifies lysine 20 of histone H4 and is associated with silent chromatin. , 2002, Molecular cell.