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Nature (London), ISSN 1476-4687, 12/2015, Volume 529, Issue 7584, pp. 110 - 114
Gain-of-function IDH mutations are initiating events that define major clinical and prognostic classes of gliomas(1,2). Mutant IDH protein produces a new... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Chromatin - metabolism | Up-Regulation | Humans | Glioma - genetics | Base Sequence | Glioma - pathology | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Binding Sites | Chromatin - drug effects | Repressor Proteins - metabolism | Oncogenes - genetics | Insulator Elements - genetics | Glioma - enzymology | Chromosomal Proteins, Non-Histone - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Isocitrate Dehydrogenase - genetics | DNA Methylation - genetics | Down-Regulation - drug effects | Mutation - genetics | CRISPR-Cas Systems - genetics | Insulator Elements - drug effects | Phenotype | Isocitrate Dehydrogenase - chemistry | Receptor, Platelet-Derived Growth Factor alpha - genetics | CCCTC-Binding Factor | CpG Islands - genetics | Protein Binding | Isocitrate Dehydrogenase - metabolism | Cell Proliferation - drug effects | Enhancer Elements, Genetic - genetics | Glutarates - metabolism | Cell Transformation, Neoplastic - drug effects | Chromatin - genetics | DNA Methylation - drug effects | Glioma - drug therapy | Complications and side effects | Care and treatment | Platelet-derived growth factor | Gliomas | Analysis | Influence | Genetic aspects | Research | Methylation | Oncogenes | DNA methylation | Epigenetics | Genomes | Mutation | Gene expression | Binding sites | Deoxyribonucleic acid--DNA | Tumors | Index Medicus
Journal Article
Nature (London), ISSN 1476-4687, 06/2017, Volume 546, Issue 7658, pp. 431 - 435
Therapies that target signalling molecules that are mutated in cancers can often have substantial short-term effects, but the emergence of resistant cancer cells is a major barrier to full cures(1,2... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Transcription, Genetic - drug effects | Humans | Male | Transcription Factor AP-1 - metabolism | DNA-Binding Proteins - metabolism | Melanoma - genetics | Female | Indoles - pharmacology | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | SOXE Transcription Factors - deficiency | Single-Cell Analysis | Cellular Reprogramming - genetics | ErbB Receptors - metabolism | In Situ Hybridization, Fluorescence | Nuclear Proteins - metabolism | Signal Transduction - genetics | Melanoma - pathology | Sulfonamides - pharmacology | Cellular Reprogramming - drug effects | Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Genetic Markers - drug effects | Vemurafenib | Drug Resistance, Neoplasm - genetics | Animals | Signal Transduction - drug effects | Genetic Markers - genetics | Cell Line, Tumor | Oncogene Protein p65(gag-jun) - metabolism | Drug Resistance, Neoplasm - drug effects | SOXE Transcription Factors - genetics | Antimitotic agents | Cell interaction | Dosage and administration | Antineoplastic agents | Drug resistance | Observations | Health aspects | Subpopulations | Transcription factors | Substance abuse treatment | Variability | Activator protein 1 | Melanoma | Genomes | Kinases | Gene expression | Sox10 protein | Signal transduction | Signaling | Converting | Population | Mutation | Differentiation | Deoxyribonucleic acid--DNA | Cancer | Index Medicus
Journal Article
BMC genomics, ISSN 1471-2164, 07/2015, Volume 16, Issue 1, pp. 517 - 517
.... Importantly, these receptors differ in their downstream adaptor molecules. Thus far, only a few studies have investigated the effects of TLR3 and TLR4 in macrophages... 
RNA sequencing | Innate immunity | Gene regulation | Toll-like receptor | Microglia | Genetics & Heredity | Life Sciences & Biomedicine | Biotechnology & Applied Microbiology | Science & Technology | Microglia - metabolism | Transcription, Genetic - drug effects | Transcription Initiation Site - drug effects | Immunity, Innate - genetics | Interferon Regulatory Factor-3 - genetics | Transcription Initiation Site - physiology | Inflammation Mediators - metabolism | Interferon-beta - genetics | Epigenesis, Genetic - drug effects | Toll-Like Receptor 3 - genetics | Immunity, Innate - drug effects | Microglia - drug effects | Gene Expression Regulation - genetics | RNA Processing, Post-Transcriptional - drug effects | Toll-Like Receptor 4 - genetics | Up-Regulation - genetics | Signal Transduction - genetics | Transcriptome - drug effects | Transcriptome - genetics | Gene Expression Regulation - drug effects | Up-Regulation - drug effects | Macrophages - metabolism | Animals | RNA Processing, Post-Transcriptional - genetics | Signal Transduction - drug effects | Epigenesis, Genetic - genetics | Lipopolysaccharides - pharmacology | Ligands | Macrophages - drug effects | Mice | Transcription, Genetic - genetics | Epigenetic inheritance | Immune response | Methyltransferases | Genes | DNA binding proteins | Nucleotide sequencing | Genetic transcription | Macrophages | Health aspects | DNA sequencing | Index Medicus
Journal Article
PloS one, ISSN 1932-6203, 04/2013, Volume 8, Issue 4, pp. e61807 - e61807
The Notch pathway can have both oncogenic and tumor suppressor roles, depending on cell context. For example, Notch signaling promotes T cell differentiation... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Transcription, Genetic - drug effects | Apoptosis - drug effects | Receptors, Notch - metabolism | Humans | Apoptosis - genetics | Receptors, Notch - genetics | Gene Expression Profiling | Hematopoiesis - drug effects | Basic Helix-Loop-Helix Transcription Factors - metabolism | T-Lymphocytes - metabolism | Serrate-Jagged Proteins | T-Lymphocytes - drug effects | B-Lymphocytes - pathology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - blood | B-Lymphocytes - metabolism | Repressor Proteins - metabolism | Bone Marrow - drug effects | Jagged-1 Protein | Basic Helix-Loop-Helix Transcription Factors - genetics | Membrane Proteins - genetics | Gene Expression Regulation, Leukemic - drug effects | Leukemia, B-Cell - pathology | Repressor Proteins - genetics | Hematopoiesis - genetics | Signal Transduction - genetics | Azacitidine - pharmacology | Leukemia, B-Cell - blood | Leukemia, B-Cell - genetics | Signal Transduction - drug effects | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics | Cell Line, Tumor | Histones - metabolism | DNA Methylation - drug effects | Calcium-Binding Proteins - genetics | Gene Silencing - drug effects | Blood Cells - metabolism | Cell Lineage - drug effects | Intercellular Signaling Peptides and Proteins - metabolism | Epigenesis, Genetic - drug effects | Membrane Proteins - metabolism | T-Lymphocytes - pathology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology | Blood Cells - drug effects | Hydroxamic Acids - pharmacology | Cell Lineage - genetics | Calcium-Binding Proteins - metabolism | Intercellular Signaling Peptides and Proteins - genetics | Azacitidine - analogs & derivatives | DNA Methylation - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | B-Lymphocytes - drug effects | Bone Marrow - pathology | Receptor, Notch3 | Cell Proliferation - drug effects | Sulfites | Epigenetic inheritance | DNA microarrays | Genes | Genetic aspects | Genetic engineering | Acute lymphocytic leukemia | B cells | T cells | Methylation | Cell differentiation | Biotechnology | Transcription factors | Bisulfite | Pathogenesis | Leukemia | Differentiation (biology) | Lymphocytes T | Kinases | Inactivation | Signal transduction | Restoration | Lymphocytes | DNA methylation | Bone marrow | Tumorigenesis | Acetylation | Deoxyribonucleic acid--DNA | CpG islands | Acute lymphatic leukemia | Deactivation | Lymphatic leukemia | Tumor cell lines | Gene silencing | Signaling | Lymphocytes B | Regulatory mechanisms (biology) | Stem cells | Epigenetics | Ligands | Tumor suppressor genes | Leukemogenesis | Lymphomas | Notch protein | Aberration | Apoptosis | Cancer | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
Nature (London), ISSN 0028-0836, 03/2012, Volume 483, Issue 7388, pp. 222 - 226
Cognitive decline is a debilitating feature of most neurodegenerative diseases of the central nervous system, including Alzheimer's disease(1). The causes... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Memory Disorders - physiopathology | Alzheimer Disease - complications | Memory Disorders - genetics | Peptide Fragments - toxicity | Humans | Neuronal Plasticity - drug effects | Receptors, Glucocorticoid - metabolism | Hippocampus - drug effects | RNA Polymerase II - metabolism | Memory Disorders - complications | Promoter Regions, Genetic - drug effects | Promoter Regions, Genetic - genetics | Gene Knockdown Techniques | Brain - metabolism | Neuronal Plasticity - genetics | Epigenesis, Genetic - drug effects | Phosphorylation - drug effects | Disease Models, Animal | Hydrogen Peroxide - toxicity | Histone Deacetylase 2 - genetics | Alzheimer Disease - physiopathology | Amyloid beta-Peptides - toxicity | Brain - physiopathology | Neurodegenerative Diseases - genetics | Neurodegenerative Diseases - complications | Brain - drug effects | Gene Expression Regulation - drug effects | Hippocampus - metabolism | Acetylation - drug effects | Animals | Neurodegenerative Diseases - physiopathology | Histone Deacetylase 2 - deficiency | Mice | Histone Deacetylase 2 - metabolism | Histones - metabolism | Alzheimer Disease - genetics | Epigenetic inheritance | Complications and side effects | Causes of | Nervous system | Genetic aspects | Degeneration | Cognition disorders | Health aspects | Epigenetics | Genetics | RNA polymerase | Kinases | Neurodegeneration | Cyclin-dependent kinases | Index Medicus
Journal Article
The New phytologist, ISSN 0028-646X, 03/2010, Volume 185, Issue 4, pp. 1108 - 1118
... or a downstream consequence of genetic variation between individuals. Genetically identical apomictic dandelion... 
Ecological genetics | Genetic inheritance | Genetic variation | DNA | Plant genetics | Epigenetics | Evolutionary genetics | Genetic loci | Plants | Methylation | apomixis | methylation‐sensitive amplified fragment length polymorphism | DNA methylation | salicylic acid | Taraxacum officinale (dandelion) | epigenetic inheritance | jasmonic acid | abiotic stress | Epigenetic inheritance | Salicylic acid | Abiotic stress | Apomixis | Methylation-sensitive amplified fragment length polymorphism | Jasmonic acid | Life Sciences & Biomedicine | Plant Sciences | Science & Technology | Reproduction, Asexual - drug effects | Taraxacum - physiology | Inheritance Patterns - drug effects | Sodium Chloride - pharmacology | Stress, Physiological - genetics | Taraxacum - drug effects | Genotype | DNA Methylation - genetics | Cyclopentanes - pharmacology | Genetic Markers | Reproduction, Asexual - genetics | Salicylic Acid - pharmacology | Genetic Variation - drug effects | Taraxacum - genetics | Oxylipins - pharmacology | Inheritance Patterns - genetics | Epigenesis, Genetic - drug effects | Stress, Physiological - drug effects | DNA Methylation - drug effects | Amplified Fragment Length Polymorphism Analysis | Ecology | Disease transmission | Genomics | Index Medicus | genome | disease resistance | arabidopsis-thaliana | hypomethylation | phenotypic plasticity | gene-expression | transposable elements | tobacco plants | plant evolution
Journal Article
Nature (London), ISSN 1476-4687, 01/2016, Volume 529, Issue 7586, pp. 413 - 417
... (Supplementary Table 1). Potent inhibitory effects were observed preferentially in TNBC lines, compared to more resistant luminal lines (Fig. 1a). Analysis of potency... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Chromatin - metabolism | Transcription, Genetic - drug effects | Humans | Transcription Factors - deficiency | Triple Negative Breast Neoplasms - drug therapy | Genome, Human - drug effects | Nuclear Proteins - deficiency | Protein Binding - drug effects | Triple Negative Breast Neoplasms - pathology | Female | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Phosphorylation - drug effects | Nuclear Proteins - genetics | Triazoles - therapeutic use | Cell Proliferation - genetics | Mediator Complex Subunit 1 - metabolism | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Transcription Factors - genetics | Phosphoserine - metabolism | Genome, Human - genetics | Azepines - therapeutic use | Azepines - pharmacology | Binding, Competitive - drug effects | Transcription Factors - metabolism | Triazoles - pharmacology | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Animals | Triple Negative Breast Neoplasms - genetics | Epigenesis, Genetic - genetics | Triple Negative Breast Neoplasms - metabolism | Nuclear Proteins - antagonists & inhibitors | Protein Phosphatase 2 - metabolism | Proteomics | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Chromatin - genetics | Casein Kinase II - metabolism | Drug Resistance, Neoplasm - drug effects | Protein Structure, Tertiary - drug effects | Antimitotic agents | Enzyme inhibitors | Patient outcomes | Breast cancer | Dosage and administration | Drug therapy | Antineoplastic agents | Studies | Inhibitor drugs | Drug resistance | Gene expression | Drug dosages | Index Medicus
Journal Article