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Cancer Cell, ISSN 1535-6108, 2011, Volume 19, Issue 1, pp. 17 - 30
and mutations occur frequently in gliomas and acute myeloid leukemia, leading to simultaneous loss and gain of activities in the production of α-ketoglutarate... 
BREAST-CANCER | TRANSCRIPTIONAL ACTIVITY | IDH2 MUTATIONS | ONCOLOGY | PROLYL HYDROXYLATION | INTEGRATED GENOMIC ANALYSIS | 2-OXOGLUTARATE OXYGENASES | ACUTE MYELOID-LEUKEMIA | HIF-ALPHA | HISTONE DEMETHYLATION | FAMILY | CELL BIOLOGY | Dioxygenases - metabolism | Histone Demethylases - antagonists & inhibitors | Gene Expression - genetics | Caenorhabditis elegans Proteins - chemistry | Humans | Ketoglutaric Acids - chemistry | Glioma - genetics | F-Box Proteins | Oxidoreductases, N-Demethylating - antagonists & inhibitors | Ketoglutaric Acids - pharmacology | Cytosine - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Glutarates - chemistry | Oxidoreductases, N-Demethylating - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Glioma - enzymology | Endostatins - metabolism | Models, Molecular | Isocitrate Dehydrogenase - genetics | Histone Demethylases - metabolism | Dioxygenases - antagonists & inhibitors | Amino Acid Substitution - physiology | Procollagen-Proline Dioxygenase - genetics | Cell Line, Tumor | Isocitrate Dehydrogenase - metabolism | Glutarates - pharmacology | Histones - metabolism | Jumonji Domain-Containing Histone Demethylases - metabolism | Caenorhabditis elegans - enzymology | Cytosine - analogs & derivatives | Gene Expression - drug effects | Caenorhabditis elegans Proteins - metabolism | Isocitrate Dehydrogenase - antagonists & inhibitors | Glioma - metabolism | Procollagen-Proline Dioxygenase - metabolism | DNA-Binding Proteins - metabolism | Mixed Function Oxygenases | Biocatalysis - drug effects | Jumonji Domain-Containing Histone Demethylases - antagonists & inhibitors | Jumonji Domain-Containing Histone Demethylases - chemistry | Procollagen-Proline Dioxygenase - antagonists & inhibitors | Ketoglutaric Acids - metabolism | Oxalates - pharmacology | Binding, Competitive | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Catalytic Domain | Proto-Oncogene Proteins - genetics | Hypoxia-Inducible Factor-Proline Dioxygenases | DNA-Binding Proteins - genetics | Homeodomain Proteins - genetics | Animals | 5-Methylcytosine - metabolism | Caenorhabditis elegans Proteins - antagonists & inhibitors | Glutarates - metabolism | Index Medicus
Journal Article
Journal of Medicinal Chemistry, ISSN 0022-2623, 02/2016, Volume 59, Issue 4, pp. 1271 - 1298
Bromodomains, small protein modules that recognize acetylated lysine on histones, play a significant role in the epigenome, where they function as "readers"... 
CHEMISTRY, MEDICINAL | SWI/SNF COMPLEXES | SMALL-MOLECULE INHIBITORS | PROSTATE-CANCER | SELECTIVE INHIBITORS | GENE-EXPRESSION | CHEMICAL PROBE | TUMOR-SUPPRESSOR | BET INHIBITORS | HISTONE ACETYLTRANSFERASE | PHD FINGER | Small Molecule Libraries - pharmacology | Antigens, Nuclear - metabolism | Humans | Drug Discovery - methods | CREB-Binding Protein - antagonists & inhibitors | Chromosomal Proteins, Non-Histone - antagonists & inhibitors | DNA-Binding Proteins - metabolism | CREB-Binding Protein - metabolism | Protein Processing, Post-Translational - drug effects | Adaptor Proteins, Signal Transducing - antagonists & inhibitors | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Lysine - metabolism | Protein-Serine-Threonine Kinases - metabolism | RNA-Binding Proteins - antagonists & inhibitors | Nerve Tissue Proteins - antagonists & inhibitors | ATPases Associated with Diverse Cellular Activities | DNA-Binding Proteins - antagonists & inhibitors | Chromosomal Proteins, Non-Histone - metabolism | Carrier Proteins - antagonists & inhibitors | Adenosine Triphosphatases - metabolism | Models, Molecular | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Adenosine Triphosphatases - antagonists & inhibitors | DNA Helicases - metabolism | Small Molecule Libraries - chemistry | Acetylation - drug effects | Animals | Carrier Proteins - metabolism | Nuclear Proteins - antagonists & inhibitors | DNA Helicases - antagonists & inhibitors | Histones - metabolism | Adaptor Proteins, Signal Transducing - metabolism | RNA-Binding Proteins - metabolism | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 07/2016, Volume 535, Issue 7610, pp. 111 - 116
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 01/2014, Volume 21, Issue 1, pp. 79 - 91
The immunogenic demise of cancer cells can be induced by various chemotherapeutics, such as anthracyclines and oxaliplatin, and provokes an immune response... 
quinacrine | apoptosis | U2OS cells | caspases | endoplasmic reticulum stress | Beclin 1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | RELEASE | AUTOPHAGY | CLEAVAGE | CHEMOTHERAPY | CELL BIOLOGY | CALRETICULIN EXPOSURE | PANNEXIN 1 | ASSAYS | FIND-ME SIGNAL | Connexins - antagonists & inhibitors | RNA-Binding Proteins - genetics | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Humans | Cell Death - immunology | rho-Associated Kinases - antagonists & inhibitors | Antineoplastic Agents - toxicity | DNA-Binding Proteins - metabolism | Lysosomes - metabolism | Lysosomal-Associated Membrane Protein 1 - genetics | Myosin Type II - metabolism | RNA Interference | rho-Associated Kinases - metabolism | Adenosine Triphosphate - metabolism | HMGB1 Protein - metabolism | Cell Membrane - metabolism | Cell Death - drug effects | RNA-Binding Proteins - antagonists & inhibitors | Nerve Tissue Proteins - antagonists & inhibitors | DNA-Binding Proteins - antagonists & inhibitors | Connexins - genetics | rho-Associated Kinases - genetics | Lysosomal-Associated Membrane Protein 1 - antagonists & inhibitors | Microtubule-Associated Proteins - antagonists & inhibitors | DNA-Binding Proteins - genetics | Nerve Tissue Proteins - genetics | Connexins - metabolism | Nerve Tissue Proteins - metabolism | Animals | Autophagy-Related Protein 5 | Cell Line, Tumor | Lysosomal-Associated Membrane Protein 1 - metabolism | Mice | RNA-Binding Proteins - metabolism | RNA, Small Interfering - metabolism | Index Medicus | Original Paper
Journal Article
The Journal of Immunology, ISSN 0022-1767, 01/2004, Volume 172, Issue 1, pp. 567 - 576
The signaling mechanism by which the anti-inflammatory cytokine IL-10 mediates suppression of proinflammatory cytokine synthesis remains largely unknown.... 
RHEUMATOID-ARTHRITIS | TUMOR-NECROSIS-FACTOR | DNA-BINDING | HUMAN NEUTROPHILS | TYROSINE PHOSPHORYLATION | INTERLEUKIN-10 RECEPTOR | GENE-EXPRESSION | KAPPA-B-ALPHA | IMMUNOLOGY | HUMAN MONOCYTES | MONONUCLEAR PHAGOCYTES | Protein Binding - genetics | Protein Biosynthesis | Interleukin-6 - antagonists & inhibitors | Humans | Tumor Necrosis Factor-alpha - genetics | Immunoglobulins - genetics | Lipopolysaccharides - antagonists & inhibitors | RNA, Messenger - metabolism | Suppressor of Cytokine Signaling Proteins | Repressor Proteins - antagonists & inhibitors | Antigens, CD - metabolism | Trans-Activators - physiology | Protein Tyrosine Phosphatases - antagonists & inhibitors | RNA, Messenger - biosynthesis | Protein Tyrosine Phosphatases - genetics | Inflammation Mediators - physiology | Glycoproteins - genetics | DNA-Binding Proteins - physiology | Protein Tyrosine Phosphatases - biosynthesis | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction - genetics | DNA - metabolism | Down-Regulation - genetics | Macrophages - metabolism | Protein Tyrosine Phosphatase, Non-Receptor Type 2 | Repressor Proteins - biosynthesis | Up-Regulation - immunology | Interleukin-10 - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Adenoviruses, Human - genetics | Interleukin-10 - immunology | Tumor Necrosis Factor-alpha - biosynthesis | Phosphorylation | Tissue Inhibitor of Metalloproteinase-1 - biosynthesis | Antigens, CD - biosynthesis | Receptors, Cell Surface | Receptors, IgG - biosynthesis | Receptors, IgG - antagonists & inhibitors | Interleukin-10 - physiology | Signal Transduction - immunology | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Signaling Lymphocytic Activation Molecule Family Member 1 | Receptors, Tumor Necrosis Factor - antagonists & inhibitors | RNA, Messenger - antagonists & inhibitors | Receptors, Tumor Necrosis Factor, Type II | Trans-Activators - genetics | Inflammation Mediators - antagonists & inhibitors | Trans-Activators - biosynthesis | Immunoglobulins - biosynthesis | Macrophages - immunology | Inflammation Mediators - immunology | Receptors, Tumor Necrosis Factor - metabolism | Immune Sera - pharmacology | Proteins - physiology | Cells, Cultured | Glycoproteins - antagonists & inhibitors | Histocompatibility Antigens Class II - biosynthesis | Tissue Inhibitor of Metalloproteinase-1 - antagonists & inhibitors | Transcription Factors - antagonists & inhibitors | Transcription Factors - biosynthesis | Up-Regulation - genetics | DNA-Binding Proteins - genetics | DNA - antagonists & inhibitors | Glycoproteins - biosynthesis | Suppressor of Cytokine Signaling 3 Protein | Down-Regulation - immunology | Interleukin-6 - biosynthesis | Receptors, Tumor Necrosis Factor - biosynthesis | STAT3 Transcription Factor | Trans-Activators - antagonists & inhibitors | Genetic Vectors | DNA-Binding Proteins - biosynthesis | Tumor Necrosis Factor-alpha - antagonists & inhibitors | SOCS-3 protein | Index Medicus | Abridged Index Medicus
Journal Article
Nature, ISSN 0028-0836, 10/2015, Volume 526, Issue 7571, pp. 136 - 139
Journal Article
Nature, ISSN 0028-0836, 03/2012, Volume 483, Issue 7391, pp. 598 - 602
Generation of induced pluripotent stem cells (iPSCs) by somatic cell reprogramming involves global epigenetic remodelling(1). Whereas several proteins are... 
CELLS | LEUKEMIA | PRC2 | HISTONE METHYLATION | MULTIDISCIPLINARY SCIENCES | PLURIPOTENT | Chromatin - metabolism | Homeodomain Proteins - metabolism | Humans | Methyltransferases - metabolism | Methyltransferases - genetics | Methyltransferases - biosynthesis | YY1 Transcription Factor - metabolism | Repressor Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Kruppel-Like Transcription Factors - metabolism | YY1 Transcription Factor - antagonists & inhibitors | Induced Pluripotent Stem Cells - cytology | Cellular Reprogramming - genetics | Repressor Proteins - metabolism | Fibroblasts - metabolism | Induced Pluripotent Stem Cells - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Nanog Homeobox Protein | Transcription Factors - antagonists & inhibitors | DNA Methylation - genetics | Polycomb-Group Proteins | Proto-Oncogene Proteins c-myc - metabolism | Enhancer of Zeste Homolog 2 Protein | Transcription Factors - metabolism | Polycomb Repressive Complex 2 | Methyltransferases - antagonists & inhibitors | Fibroblasts - cytology | RNA, Small Interfering | Histones - metabolism | Methylation | Chromatin - genetics | RNA-Binding Proteins - metabolism | Physiological aspects | Chromatin | Genetic aspects | Research | Methyltransferases | Embryonic stem cells | Enzymes | Efficiency | Stem cells | Epigenetics | Kinases | Gene expression | Apoptosis | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 08/2010, Volume 466, Issue 7309, pp. 941 - 946
DNA double-strand breaks (DSBs) pose a potent threat to genome integrity. These lesions also contribute to the efficacy of radiotherapy and many cancer... 
REPAIR PROTEINS | COMPLEX | ENZYME | SPECIFICITY | STRUCTURAL BASIS | MULTIDISCIPLINARY SCIENCES | DOUBLE-STRAND BREAKS | CHAINS | MAMMALIAN-CELLS | BINDING | STATISTICAL-MODEL | Chromatin - metabolism | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | DNA Repair - physiology | Ubiquitin - metabolism | Ubiquitin-Protein Ligases - antagonists & inhibitors | DNA Breaks, Double-Stranded | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Cysteine Endopeptidases - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cysteine Endopeptidases - deficiency | Ubiquitination - physiology | Protein-Serine-Threonine Kinases - metabolism | Chromatin - chemistry | Cell Line | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Cell Cycle Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | Ubiquitin - genetics | Ataxia Telangiectasia Mutated Proteins | Ubiquitin-Conjugating Enzymes - metabolism | Cysteine Endopeptidases - genetics | Cell Line, Tumor | Protein Binding | Ubiquitin-Conjugating Enzymes - antagonists & inhibitors | Ubiquitin-Protein Ligases - genetics | Ubiquitin | Amino acids | Genetic aspects | Models | Chemical properties | DNA damage | Proteins | Enzymes | Genetics | Mutation | DNA repair | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 02/2013, Volume 494, Issue 7438, pp. 502 - 505
Mammalian telomeres repress DNA-damage activation at natural chromosome ends by recruiting specific inhibitors of the DNA-damage machinery that form a... 
UBIQUITINATION | RECOMBINATION | MAINTENANCE | COMPLEX | REPAIR | MAMMALIAN TELOMERES | MULTIDISCIPLINARY SCIENCES | DNA-DAMAGE | CELL-CYCLE | PROTEINS | TRF2 | Tumor Suppressor Proteins - antagonists & inhibitors | Chromosomes, Mammalian - genetics | Protein Multimerization | Ubiquitin-Protein Ligases - antagonists & inhibitors | Telomeric Repeat Binding Protein 2 - chemistry | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Telomere - metabolism | Protein-Serine-Threonine Kinases - metabolism | Telomere - genetics | Protein Structure, Tertiary | Endopeptidases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Chromosomal Proteins, Non-Histone - metabolism | Signal Transduction | Cell Cycle Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | Ataxia Telangiectasia Mutated Proteins | Endopeptidases - deficiency | Protein Transport | Animals | DNA Repair | Telomeric Repeat Binding Protein 2 - metabolism | Mice | DNA Damage | Enzyme Activation | Tumor Suppressor p53-Binding Protein 1 | Chromosomes, Mammalian - metabolism | Telomeres | Research | Binding proteins | Observations | Properties | DNA damage | Proteins | Enzymes | DNA methylation | Amino acids | Agreements | Telomerase | Chromosomes | Index Medicus | RNF168 | Brca1 | genomic stability | telomere | ATM | NHEJ
Journal Article
Nature, ISSN 0028-0836, 09/2016, Volume 538, Issue 7623, pp. 114 - 117
The common participation of oncogenic KRAS proteins in many of the most lethal human cancers, together with the ease of detecting somatic KRAS mutant alleles... 
TARGET | CRM1/XPO1 | ACTIVATION | MODELS | MULTIDISCIPLINARY SCIENCES | KINASE | YAP | MUTATIONS | INHIBITORS | IDENTIFICATION | Lung Neoplasms - drug therapy | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Lung Neoplasms - metabolism | Cell Survival - genetics | Lung Neoplasms - pathology | NF-kappa B - metabolism | Phosphoproteins - antagonists & inhibitors | Phosphoproteins - metabolism | DNA-Binding Proteins - metabolism | Cell Nucleus - metabolism | RNA Interference | Adaptor Proteins, Signal Transducing - antagonists & inhibitors | Female | Verteporfin | Protein-Serine-Threonine Kinases - metabolism | Carcinoma, Non-Small-Cell Lung - pathology | Follistatin-Related Proteins - genetics | Lung Neoplasms - genetics | Cell Survival - drug effects | NF-kappa B - antagonists & inhibitors | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | Carcinoma, Non-Small-Cell Lung - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Porphyrins - pharmacology | Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Animals | Karyopherins - metabolism | Active Transport, Cell Nucleus - drug effects | Genes, Lethal - genetics | NF-KappaB Inhibitor alpha - metabolism | Nuclear Proteins - antagonists & inhibitors | Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | RNA, Small Interfering | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Cell Nucleus - drug effects | Karyopherins - antagonists & inhibitors | Receptors, Cytoplasmic and Nuclear - metabolism | Care and treatment | Genetic aspects | Gene mutations | Health aspects | Guanosine triphosphatase | Lung cancer | Genomics | Genomes | Kinases | Drug resistance | Gene expression | Drug dosages | Index Medicus
Journal Article