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Nature (London), ISSN 1476-4687, 2012, Volume 487, Issue 7408, pp. 443 - 448
Journal Article
Nature structural & molecular biology, ISSN 1545-9985, 2014, Volume 21, Issue 7, pp. 617 - 625
Nucleosomes are the fundamental unit of chromatin, but analysis of transcription-independent nucleosome functions has been complicated by the gene-expression... 
MITOSIS | XENOPUS EGG EXTRACTS | DNA INTERACTIONS | BIOPHYSICS | MITOTIC CHROMOSOME | KINASE AURORA-B | BIOCHEMISTRY & MOLECULAR BIOLOGY | RAN GTPASE | ENVELOPE | AUTOINTEGRATION FACTOR BAF | CHROMOSOMAL PASSENGER COMPLEX | CELL BIOLOGY | Guanine Nucleotide Exchange Factors - physiology | Xenopus Proteins - genetics | DNA-Binding Proteins - metabolism | Spindle Apparatus - metabolism | Guanine Nucleotide Exchange Factors - metabolism | Cell Cycle Proteins - genetics | Nuclear Proteins - genetics | DNA-Binding Proteins - physiology | Guanine Nucleotide Exchange Factors - genetics | Transcription Factors - physiology | Xenopus laevis | Cell Cycle Proteins - metabolism | Chromatin Assembly and Disassembly | Nucleosomes - metabolism | Nuclear Proteins - metabolism | Nucleosomes - physiology | DNA - metabolism | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Nuclear Pore - metabolism | Transcription Factors - metabolism | Nuclear Envelope - metabolism | Animals | Proteomics | Xenopus Proteins - physiology | Xenopus Proteins - metabolism | Models, Genetic | Nuclear Proteins - physiology | Histones - metabolism | Cell Cycle Proteins - physiology | Chromatin | DNA replication | DNA damage | Physiological aspects | Genetic aspects | Research | Amphibians | Gene expression | Molecular biology | Deoxyribonucleic acid--DNA
Journal Article
Journal Article
Journal Article
PloS one, ISSN 1932-6203, 2017, Volume 12, Issue 1, p. e0169648
The structural maintenance of chromosome 5/6 complex (Smc5/6) is a restriction factor that represses hepatitis B virus (HBV) transcription. HBV counters this... 
CELLS | NUCLEAR-BODIES | HEPATITIS-B-VIRUS | REPLICATION | DNA | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | EPIGENETIC REGULATION | COMPONENTS | BINDING | HUMANIZED MICE | Autoantigens - metabolism | Hepatitis B - metabolism | Antigens, Nuclear - metabolism | Humans | Hepatitis B - virology | Male | Hepatocytes - metabolism | Autoantigens - genetics | Hepatitis B - immunology | Hepatocytes - cytology | Trans-Activators - genetics | Cell Cycle Proteins - genetics | Promyelocytic Leukemia Protein - metabolism | Nuclear Proteins - genetics | Cytokines - genetics | Hepatitis B virus - immunology | Promyelocytic Leukemia Protein - genetics | Cytokines - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Chromosomal Proteins, Non-Histone | Nuclear Proteins - metabolism | Mice, SCID | Immunity, Innate - immunology | Animals | Antigens, Nuclear - genetics | Virus Replication | Trans-Activators - metabolism | Mice | Immune response | Analysis | Genetic aspects | Hepatitis B virus | Research | Genetic transcription | Hepatitis B | Cell culture | HBX protein | Pathogenesis | Viruses | Infections | Genomes | Degradation | Proteins | Hepatitis | Hepatology | Localization | Bioinformatics | Chromosomes | Deoxyribonucleic acid--DNA | Immune system | Antigens | Cytokines | Chromosome 5 | Gene expression | Ribonucleic acid--RNA | Hepatocytes | Interferon | Kinetics | RNA | Deoxyribonucleic acid | Ribonucleic acid
Journal Article
Journal Article
Nature (London), ISSN 1476-4687, 2016, Volume 534, Issue 7605, pp. 55 - 62
Somatic mutations have been extensively characterized in breast cancer, but the effects of these genetic alterations on the proteomic landscape remain poorly... 
PATHWAYS | HETEROGENEITY | PIK3CA MUTATIONS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | GENES | BIOLOGY | RECEPTOR | EXPRESSION | SIGNATURE | REVEALS | Protein Kinases - metabolism | Focal Adhesion Kinase 1 - genetics | Receptor, Epidermal Growth Factor - genetics | Protein Kinases - genetics | Cyclin-Dependent Kinases - metabolism | Receptor, ErbB-2 - genetics | Receptors, G-Protein-Coupled - metabolism | Genomics | Humans | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Phosphoproteins - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - metabolism | Breast Neoplasms - enzymology | Receptor, Epidermal Growth Factor - metabolism | Phosphoproteins - analysis | Mass Spectrometry | src-Family Kinases - metabolism | Female | Cyclin-Dependent Kinases - genetics | Focal Adhesion Kinase 1 - metabolism | Chromosomes, Human, Pair 5 - genetics | Breast Neoplasms - classification | Chromosome Deletion | p21-Activated Kinases - genetics | Signal Transduction | Molecular Sequence Annotation | Calcium-Binding Proteins - deficiency | Phosphoproteins - genetics | Mutation - genetics | S-Phase Kinase-Associated Proteins - metabolism | p21-Activated Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Proteomics | S-Phase Kinase-Associated Proteins - genetics | Receptors, G-Protein-Coupled - genetics | src-Family Kinases - genetics | Calcium-Binding Proteins - genetics | Breast cancer | Genetic aspects | Research | Oncology, Experimental | Cancer | Physiological aspects | Methods | Mutation (Biology) | Proteins | Gene amplification | Peptides | Protein expression | Genomes | Mutation | Kinases | Deoxyribonucleic acid--DNA | Tumors
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2011, Volume 108, Issue 36, pp. 14944 - 14949
The bacterial pathogen Helicobacter pylori chronically infects the human gastric mucosa and is the leading risk factor for the development of gastric cancer.... 
Helicobacter pylori | Epithelial cells | DNA damage | DNA | Cell nucleus | Cell lines | Bacteria | Cultured cells | Infections | Mice | Chromosome breaks | DNA damage signaling | Gastric tumorigenesis | Genomic instability | CYTOLETHAL DISTENDING TOXIN | MULTIDISCIPLINARY SCIENCES | RISK | MISMATCH REPAIR | COLONIZATION | GENETIC INSTABILITY | EPITHELIAL-CELLS | chromosome breaks | GASTRIC-CANCER | INFLAMMATION | INFECTION | MICE | genomic instability | gastric tumorigenesis | Phosphorylation | Epithelial Cells - metabolism | Humans | Stomach Neoplasms - metabolism | Helicobacter Infections - complications | Stomach Neoplasms - pathology | Intracellular Signaling Peptides and Proteins - metabolism | Antigens, Bacterial - genetics | DNA Breaks, Double-Stranded | Helicobacter Infections - pathology | DNA-Binding Proteins - metabolism | Tumor Suppressor Proteins - genetics | Trans-Activators - genetics | Cell Cycle Proteins - genetics | Helicobacter Infections - metabolism | Nuclear Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Stomach Neoplasms - genetics | Tumor Suppressor Proteins - metabolism | Chromosomal Proteins, Non-Histone - metabolism | Bacterial Proteins - genetics | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Genomic Islands | Epithelial Cells - pathology | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Chromosomal Proteins, Non-Histone - genetics | Bacterial Adhesion | Stomach Neoplasms - microbiology | Animals | Histones - genetics | Helicobacter pylori - metabolism | Epithelial Cells - microbiology | Chromosome Aberrations | Cell Line, Tumor | Bacterial Proteins - metabolism | Trans-Activators - metabolism | Histones - metabolism | Tumor Suppressor p53-Binding Protein 1 | Antigens, Bacterial - metabolism | Carcinogens | Cocarcinogens | Physiological aspects | Genetic aspects | Research | Health aspects | Cells | Biological Sciences
Journal Article