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1. Full Text Jarid2 and PRC2, partners in regulating gene expression
by Li, Gang and Margueron, Raphael and Ku, Manching and Chambon, Pierre and Bernstein, Bradley E and Reinberg, Danny
Genes and Development, ISSN 0890-9369, 02/2010, Volume 24, Issue 4, pp. 368 - 380
The Polycomb group proteins foster gene repression profiles required for proper development and unimpaired adulthood, and comprise the components of the... 
Polycomb | Chromatin | Histone methylation | Jarid2 | HISTONE METHYLTRANSFERASE ACTIVITY | DEVELOPMENTAL REGULATORS | CHROMATIN-STRUCTURE | JUMONJI GENE | POLYCOMB-REPRESSIVE COMPLEX-2 | DEVELOPMENTAL BIOLOGY | chromatin | NUCLEAR-PROTEIN | CARDIAC DEVELOPMENT | CELL BIOLOGY | TARGET GENES | EMBRYONIC STEM-CELLS | IN-VIVO | GENETICS & HEREDITY | Embryonic Stem Cells - metabolism | Embryonic Stem Cells - cytology | Polycomb-Group Proteins | Drosophila Proteins - metabolism | Nerve Tissue Proteins - genetics | Enhancer of Zeste Homolog 2 Protein | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Polycomb Repressive Complex 2 | Animals | Histone-Lysine N-Methyltransferase - metabolism | Gene Expression Regulation, Developmental | Protein Binding | Cell Differentiation | Mice | Repressor Proteins - metabolism | Analysis | Histones | Genetic aspects | Chemical properties | Gene expression | Structure | Mammals | Research Paper
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2. Full Text Mapping and analysis of chromatin state dynamics in nine human cell types
by Ernst, Jason and Kheradpour, Pouya and Mikkelsen, Tarjei S and Shoresh, Noam and Ward, Lucas D and Epstein, Charles B and Zhang, Xiaolan and Wang, Li and Issner, Robbyn and Coyne, Michael and Ku, Manching and Durham, Timothy and Kellis, Manolis and Bernstein, Bradley E
Nature, ISSN 0028-0836, 05/2011, Volume 473, Issue 7345, pp. 43 - 49
Chromatin profiling has emerged as a powerful means of genome annotation and detection of regulatory activity. The approach is especially well suited to the... 
POPULATION | METAANALYSIS | PROMOTERS | MULTIDISCIPLINARY SCIENCES | EMBRYONIC STEM-CELLS | GENE-EXPRESSION | SUSCEPTIBILITY LOCI | HISTONE MODIFICATIONS | ENHANCERS | TRANSCRIPTION-FACTOR-BINDING | GENOME-WIDE ASSOCIATION | Cell Line | Chromatin - metabolism | Reproducibility of Results | Humans | Cell Physiological Phenomena | Cells, Cultured | Gene Expression Regulation | Chromosome Mapping | Transcription Factors - genetics | Promoter Regions, Genetic - genetics | Genome, Human - genetics | Hep G2 Cells | Cell Line, Tumor | Binding Sites | Chromatin - genetics | Mechanical properties | Chromosome mapping | Chromatin | Models | Proteins | Disease | Cellular biology | Stem cells | Genomes | RNA polymerase | Gene expression | Binding sites
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3. Full Text In vitro reprogramming of fibroblasts into a pluripotent ES-cell-like state
by Meissner, Alexander and Brambrink, Tobias and Hochedlinger, Konrad and Foreman, Ruth and Ku, Manching and Jaenisch, Rudolf and Bernstein, Bradley E and Wernig, Marius
Nature, ISSN 0028-0836, 07/2007, Volume 448, Issue 7151, pp. 318 - 324
Nuclear transplantation can reprogramme a somatic genome back into an embryonic epigenetic state, and the reprogrammed nucleus can create a cloned animal or... 
SOMATIC-CELLS | DEVELOPMENTAL REGULATORS | RETROVIRAL GENOMES | CLONING | DNA | MULTIDISCIPLINARY SCIENCES | EMBRYONIC STEM-CELLS | TRANSCRIPTION | DIFFERENTIATION | DE-NOVO METHYLATION | EXPRESSION | Chromatin - metabolism | Homeodomain Proteins - metabolism | Male | Chimera - growth & development | Chimera - genetics | Teratoma - metabolism | DNA-Binding Proteins - metabolism | Octamer Transcription Factor-3 - genetics | DNA Methylation | Chimera - embryology | Female | Cell Differentiation | Fibroblasts - metabolism | Nanog Homeobox Protein | Pluripotent Stem Cells - cytology | Gene Silencing | DNA-Binding Proteins - genetics | Homeodomain Proteins - genetics | Pluripotent Stem Cells - metabolism | Cell Lineage | Teratoma - pathology | Animals | Octamer Transcription Factor-3 - metabolism | Fibroblasts - cytology | Mice | Chimera - metabolism | Chromatin - genetics | Stem cell research | Evaluation | Nucleotide sequence | Fibroblasts | Research | DNA binding proteins | Gene expression | Embryos | Deoxyribonucleic acid | Rodents | Stem cells | Ethics | Cloning | Derivation | Genomes | In vitro testing | Methylation
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4. Full Text Dissecting direct reprogramming through integrative genomic analysis
by Mikkelsen, Tarjei S and Hanna, Jacob and Zhang, Xiaolan and Ku, Manching and Wernig, Marius and Schorderet, Patrick and Bernstein, Bradley E and Jaenisch, Rudolf and Lander, Eric S and Meissner, Alexander
Nature, ISSN 0028-0836, 07/2008, Volume 454, Issue 7200, pp. 49 - 55
Somatic cells can be reprogrammed to a pluripotent state through the ectopic expression of defined transcription factors. Understanding the mechanism and... 
PLURIPOTENT STEM-CELLS | DEFINED FACTORS | MYC | MULTIDISCIPLINARY SCIENCES | MOUSE | HUMAN FIBROBLASTS | STATE | GENERATION | INDUCTION | HUMAN SOMATIC-CELLS | EXPRESSION | Cell Line | Chromatin - metabolism | Embryonic Stem Cells - metabolism | Pluripotent Stem Cells - cytology | DNA (Cytosine-5-)-Methyltransferase 1 | Genomics | Transcription Factors - deficiency | Enzyme Inhibitors - pharmacology | Genome - genetics | Gene Expression Profiling | DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors | Transcription Factors - genetics | DNA (Cytosine-5-)-Methyltransferases - metabolism | Pluripotent Stem Cells - metabolism | Azacitidine - pharmacology | Cell Lineage | DNA (Cytosine-5-)-Methyltransferases - genetics | DNA Methylation | Animals | Gene Expression Regulation, Developmental | Mice | Cellular Reprogramming - genetics | Proteins | Protease inhibitors | Cyclin-dependent kinases | Analysis | Stem cells | Dissection
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5. Full Text GC-rich sequence elements recruit PRC2 in mammalian ES cells
by Mendenhall, Eric M and Koche, Richard P and Truong, Thanh and Zhou, Vicky W and Issac, Biju and Chi, Andrew S and Ku, Manching and Bernstein, Bradley E
PLoS genetics, ISSN 1553-7390, 12/2010, Volume 6, Issue 12, pp. e1001244 - 10
Polycomb proteins are epigenetic regulators that localize to developmental loci in the early embryo where they mediate lineage-specific gene repression. In... 
POLYCOMB TARGETS | COMPLEX | DEVELOPMENTAL REGULATORS | PROTEIN | DNA METHYLATION | CHROMATIN | DROSOPHILA-MELANOGASTER | EMBRYONIC STEM-CELLS | GENETICS & HEREDITY | METHYLTRANSFERASE ACTIVITY | SELF-RENEWAL | Mammals - genetics | Embryonic Stem Cells - metabolism | Mammals - metabolism | Embryonic Stem Cells - cytology | Humans | Repressor Proteins - genetics | Polycomb-Group Proteins | GC Rich Sequence | Animals | Protein Binding | Cell Differentiation | Mice | Repressor Proteins - metabolism | Nucleotide sequence | Physiological aspects | Genetic aspects | Genomes | Research | DNA binding proteins | Embryonic stem cells | Proteins | DNA methylation | Medical research | Deoxyribonucleic acid | DNA | Stem cells
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6. Full Text Genome-wide maps of chromatin state in pluripotent and lineage-committed cells
by Mikkelsen, Tarjei S and Ku, Manching and Jaffe, David B and Issac, Biju and Lieberman, Erez and Giannoukos, Georgia and Alvarez, Pablo and Brockman, William and Kim, Tae-Kyung and Koche, Richard P and Lee, William and Mendenhall, Eric and O'Donovan, Aisling and Presser, Aviva and Russ, Carsten and Xie, Xiaohui and Meissner, Alexander and Wernig, Marius and Jaenisch, Rudolf and Nusbaum, Chad and Lander, Eric S and Bernstein, Bradley E
Nature, ISSN 0028-0836, 08/2007, Volume 448, Issue 7153, pp. 553 - 560
We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells. By... 
HISTONE LYSINE METHYLATION | DEVELOPMENTAL REGULATORS | DNA METHYLATION | NONCODING RNAS | MULTIDISCIPLINARY SCIENCES | EMBRYONIC STEM-CELLS | MOUSE | TRANSCRIPTION | GENE-EXPRESSION | DIFFERENTIATION | POLYCOMB | Chromatin - metabolism | Genomic Imprinting | Pluripotent Stem Cells - cytology | Genome - genetics | Male | Promoter Regions, Genetic - genetics | Pluripotent Stem Cells - metabolism | Animals | Gene Expression Regulation, Developmental | Alleles | CpG Islands - genetics | Fibroblasts | Mice | Histones - metabolism | Transcription, Genetic - genetics | Methylation | Chromatin - genetics | Cell Lineage - genetics | Chromatin | Genomics | Research methodology | Rodents | Stem cells
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7. Full Text Genomewide analysis of PRC1 and PRC2 occupancy identifies two classes of bivalent domains
by Ku, Manching and Koche, Richard P and Rheinbay, Esther and Mendenhall, Eric M and Endoh, Mitsuhiro and Mikkelsen, Tarjei S and Presser, Aviva and Nusbaum, Chad and Xie, Xiaohui and Chi, Andrew S and Adli, Mazhar and Kasif, Simon and Ptaszek, Leon M and Cowan, Chad A and Lander, Eric S and Koseki, Haruhiko and Bernstein, Bradley E
PLoS Genetics, ISSN 1553-7390, 10/2008, Volume 4, Issue 10, p. e1000242
In embryonic stem (ES) cells, bivalent chromatin domains with overlapping repressive (H3 lysine 27 tri-methylation) and activating (H3 lysine 4... 
GROUP PROTEINS RING1A/B | RNA-POLYMERASE-II | POLYCOMB TARGETS | DEVELOPMENTAL REGULATORS | HISTONE H2A | DROSOPHILA-MELANOGASTER | EMBRYONIC STEM-CELLS | GENETICS & HEREDITY | GENE FAMILY | NF-KAPPA-B | ES CELLS | Protein Structure, Tertiary | Chromatin - metabolism | Embryonic Stem Cells - metabolism | Promoter Regions, Genetic | Epigenesis, Genetic | Humans | Computational Biology | Repressor Proteins - genetics | Chromosome Mapping | Polycomb-Group Proteins | Pluripotent Stem Cells - metabolism | Animals | Chromatin Immunoprecipitation | CpG Islands | Mice | Histones - metabolism | Genome | Genome, Human | Methylation | Oxidoreductases, N-Demethylating - metabolism | Jumonji Domain-Containing Histone Demethylases | Repressor Proteins - metabolism | Chromatin - chemistry | Proteins | Studies | Chromatin | Genomics | Epigenetics | Genetics | Genomes | RNA polymerase | Gene expression | Islands | Molecular weight
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8. Full Text An epigenetic mechanism of resistance to targeted therapy in T cell acute lymphoblastic leukemia
by Knoechel, Birgit and Roderick, Justine E and Williamson, Kaylyn E and Zhu, Jiang and Lohr, Jens G and Cotton, Matthew J and Gillespie, Shawn M and Fernandez, Daniel and Ku, Manching and Wang, Hongfang and Piccioni, Federica and Silver, Serena J and Jain, Mohit and Pearson, Daniel and Kluk, Michael J and Ott, Christopher J and Shultz, Leonard D and Brehm, Michael A and Greiner, Dale L and Gutierrez, Alejandro and Stegmaier, Kimberly and Kung, Andrew L and Root, David E and Bradner, James E and Aster, Jon C and Kelliher, Michelle A and Bernstein, Bradley E
Nature Genetics, ISSN 1061-4036, 2014, Volume 46, Issue 4, pp. 364 - 370
The identification of activating NOTCH1 mutations in T cell acute lymphoblastic leukemia (T-ALL) led to clinical testing of g-secretase inhibitors (GSIs) that... 
NOTCH1 | INHIBITION | CHROMATIN | PATHWAY | GENES | GENETICS & HEREDITY | C-MYC | ACUTE MYELOID-LEUKEMIA | CANCER | LENTIVIRAL RNAI LIBRARY | GENOME | Chromatin - metabolism | Humans | Flow Cytometry | Chromatin Immunoprecipitation | Gene Expression Regulation, Neoplastic - drug effects | Indoles | Nuclear Proteins - genetics | Real-Time Polymerase Chain Reaction | Gene Expression Regulation, Neoplastic - genetics | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - drug therapy | Enzyme-Linked Immunosorbent Assay | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Signal Transduction - genetics | Transcription Factors - genetics | Enzyme Inhibitors - therapeutic use | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Epigenesis, Genetic - genetics | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Mice | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Histones - metabolism | Receptor, Notch1 - antagonists & inhibitors | Receptor, Notch1 - genetics | Chromatin - genetics | Care and treatment | Pharmacology, Experimental | Acute lymphocytic leukemia | Research | Drug resistance | Proteins | Genotype & phenotype | Leukemia | Epigenetics | Genomes | Kinases | Gene expression | Cancer therapies
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9. Full Text Control of Phenotypic Plasticity of Smooth Muscle Cells by Bone Morphogenetic Protein Signaling through the Myocardin-related Transcription Factors
by Giorgio Lagna and Manching M. Ku and Peter H. Nguyen and Nicole A. Neuman and Brandi N. Davis and Akiko Hata
Journal of Biological Chemistry, ISSN 0021-9258, 12/2007, Volume 282, Issue 51, pp. 37244 - 37255
Vascular smooth muscle cells (VSMCs), unlike other muscle cells, do not terminally differentiate. In response to injury, VSMCs change phenotype, proliferate,... 
GROWTH-FACTOR-BETA | SM22-ALPHA TRANSCRIPTION | HEREDITARY HEMORRHAGIC TELANGIECTASIA | BIOCHEMISTRY & MOLECULAR BIOLOGY | ARTERIAL-HYPERTENSION | VASCULAR CALCIFICATION | SERUM RESPONSE FACTOR | GENE-EXPRESSION | PRIMARY PULMONARY-HYPERTENSION | BMPR-II | DEPENDENT ACTIVATION | Oncogene Proteins, Fusion - metabolism | Muscle, Smooth, Vascular - metabolism | Humans | Actins - metabolism | Myocytes, Smooth Muscle - pathology | rhoA GTP-Binding Protein - metabolism | DNA-Binding Proteins - metabolism | Pluripotent Stem Cells - pathology | Bone Morphogenetic Proteins - metabolism | Cell Nucleus - metabolism | Cell Nucleus - pathology | Bone Morphogenetic Protein Receptors, Type II - agonists | Proto-Oncogene Proteins c-akt - metabolism | Bone Morphogenetic Proteins - pharmacology | Myocytes, Smooth Muscle - metabolism | Cell Line | Promoter Regions, Genetic | Signal Transduction | Trans-Activators | Elafin - metabolism | Hypertension, Pulmonary - metabolism | Bone Morphogenetic Protein Receptors, Type II - metabolism | Pluripotent Stem Cells - metabolism | Cell Movement - drug effects | Muscle, Smooth, Vascular - pathology | Phenotype | Cell Differentiation - drug effects | Active Transport, Cell Nucleus - drug effects | Hypertension, Pulmonary - pathology | Transforming Growth Factor beta - metabolism
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