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The Journal of immunology (1950), ISSN 1550-6606, 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
Journal Article
Oncogene, ISSN 1476-5594, 2007, Volume 26, Issue 32, pp. 4635 - 4647
...). APBs are PML bodies containing telomeric DNA and telomere-binding proteins, and are observed only in a small fraction of cells within asynchronously dividing ALT-positive cell populations... 
Telomeres | siRNA | Alternative lengthening of telomeres | Methionine restriction | PML | ALT-associated PML bodies | CANCER-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | telomeres | DNA-DAMAGE | MAMMALIAN-CELLS | PROTEIN COMPLEX | CELL BIOLOGY | HUMAN RAP1 | METABOLIC DEFECT | LARGE-BODY FORMATION | NUCLEAR-BODIES | ONCOLOGY | alternative lengthening of telomeres | methionine restriction | GENETICS & HEREDITY | PROMYELOCYTIC LEUKEMIA BODIES | TUMOR-CELL-LINES | Humans | Neoplasm Proteins - antagonists & inhibitors | Resting Phase, Cell Cycle | Autoantigens - genetics | RNA Interference | Neoplasm Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Telomeric Repeat Binding Protein 2 - antagonists & inhibitors | DNA Repair Enzymes - physiology | DNA-Binding Proteins - physiology | DNA-Binding Proteins - antagonists & inhibitors | Telomeric Repeat Binding Protein 2 - physiology | Genetic Techniques | Autoantigens - physiology | Tumor Suppressor Proteins - physiology | G1 Phase | Cell Line, Tumor | Intracellular Signaling Peptides and Proteins - physiology | Cell Cycle Proteins - physiology | Telomeric Repeat Binding Protein 1 - physiology | Tumor Suppressor Proteins - antagonists & inhibitors | Neoplasm Proteins - physiology | DNA Repair Enzymes - genetics | Telomeric Repeat Binding Protein 1 - genetics | Cell Cycle Proteins - antagonists & inhibitors | MRE11 Homologue Protein | Telomere-Binding Proteins - genetics | Tumor Suppressor Proteins - genetics | Telomere-Binding Proteins - physiology | Cell Cycle Proteins - genetics | Telomere - metabolism | DNA Repair Enzymes - antagonists & inhibitors | Nuclear Proteins - genetics | Methionine - deficiency | Telomere - genetics | Transcription Factors - physiology | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | RNA, Small Interfering - pharmacology | Antigens, Nuclear - physiology | Transcription Factors - antagonists & inhibitors | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Telomere-Binding Proteins - antagonists & inhibitors | Antigens, Nuclear - genetics | Nuclear Proteins - antagonists & inhibitors | Telomeric Repeat Binding Protein 1 - antagonists & inhibitors | Cell Proliferation - drug effects | Nuclear Proteins - physiology | Telomeric Repeat Binding Protein 2 - genetics | Tumor Suppressor p53-Binding Protein 1 | Promyelocytic Leukemia Protein | Physiological aspects | Genetic aspects | Research | Cancer cells | Proteins | Ribonucleic acid | Cell cycle | Genetics | Oncology | Ribonucleic acid--RNA | DNA repair | Cancer
Journal Article
Nature, ISSN 0028-0836, 04/2003, Volume 422, Issue 6934, pp. 905 - 909
.... Here we report a conserved nuclear protein, named Chibby, which was identified in a screen for proteins that directly interact with the C-terminal region of β-catenin... 
PROTEIN | GENE | WINGLESS SIGNAL | MULTIDISCIPLINARY SCIENCES | XENOPUS EMBRYOS | INTERFERENCE | MAMMALIAN-CELLS | EXPRESSION | DROSOPHILA | ARMADILLO | LEF-1 | Wnt1 Protein | Cytoskeletal Proteins - antagonists & inhibitors | Humans | Transcriptional Activation | Molecular Sequence Data | Wnt Proteins | Drosophila Proteins - metabolism | RNA, Messenger - metabolism | Trans-Activators - chemistry | Drosophila melanogaster - genetics | DNA-Binding Proteins - metabolism | Lymphoid Enhancer-Binding Factor 1 | Armadillo Domain Proteins | RNA Interference | Trans-Activators - genetics | Conserved Sequence | Carrier Proteins - chemistry | Cytoskeletal Proteins - metabolism | Nuclear Proteins - genetics | Binding Sites | Proto-Oncogene Proteins - metabolism | Cell Line | Proto-Oncogene Proteins - antagonists & inhibitors | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | beta Catenin | RNA, Messenger - genetics | Zebrafish Proteins | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | Transcription Factors - antagonists & inhibitors | Cytoskeletal Proteins - chemistry | Drosophila Proteins - chemistry | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Nuclear Proteins - chemistry | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Carrier Proteins - genetics | Phenotype | Animals | Carrier Proteins - metabolism | Epistasis, Genetic | Protein Binding | Trans-Activators - metabolism | Drosophila Proteins - genetics | Trans-Activators - antagonists & inhibitors | COS Cells | Proteins | Genetics | Genes | Cells
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
Journal Article
Oncogene, ISSN 0950-9232, 10/2011, Volume 30, Issue 41, pp. 4261 - 4274
In the presence of sustained DNA damage occurring in S-phase or G2, normal cells arrest before mitosis and eventually become senescent. The checkpoint kinases... 
cyclin B1 | ATM | Chk2 | G2-M checkpoint | cell cycle | GENOTOXIC STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOTIC CATASTROPHE | TRANSCRIPTIONAL REPRESSION | G CHECKPOINT | CELL BIOLOGY | GENOMIC INSTABILITY | RETINOBLASTOMA PROTEIN | ONCOLOGY | GENETICS & HEREDITY | P53-DEFICIENT CELLS | CELL-CYCLE EXIT | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | Protein Kinases - metabolism | G2 Phase Cell Cycle Checkpoints - physiology | Phosphorylation | Protein Kinases - genetics | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Immunoblotting | Male | Cyclin B1 - metabolism | Pyrones - pharmacology | Tumor Suppressor Protein p53 - genetics | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | RNA Interference | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Antineoplastic Agents - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | HCT116 Cells | Cell Cycle Proteins - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin B1 - genetics | Morpholines - pharmacology | Signal Transduction - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Piperazines - pharmacology | G2 Phase Cell Cycle Checkpoints - genetics | Signal Transduction - drug effects | Cell Line, Tumor | Checkpoint Kinase 2 | Bleomycin - pharmacology | Checkpoint Kinase 1 | Signal Transduction - physiology | DNA Damage | HeLa Cells | Cell division | Oxidative stress | Signal transduction | DNA damage | Cyclin-dependent kinases | Cell cycle | CHK2 protein | Epithelial cells | Mitosis | CHK1 protein | G2 phase | Genotoxicity | Osteosarcoma cells | p53 protein | Cyclin-dependent kinase | Chemotherapy | Fibroblasts | Cancer | Life Sciences | Biochemistry, Molecular Biology
Journal Article
Nature (London), ISSN 1476-4687, 2015, Volume 526, Issue 7571, pp. 136 - 139
Journal Article
Nature (London), ISSN 1476-4687, 2010, Volume 466, Issue 7309, pp. 941 - 946
... of ubiquitin chain linkage is key for determining the outcome of ubiquitination. For example, Lys 48 (K48)-linked Ub chains usually mark proteins for proteasomal... 
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
Journal Article
The EMBO journal, ISSN 0261-4189, 2011, Volume 30, Issue 4, pp. 770 - 782
Notch signalling is important for development and tissue homeostasis and activated in many human cancers. Nevertheless, mutations in Notch pathway components... 
miR‐200 | ZEB1 | EMT | Notch | stemness | miR-200 | STEM-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOWN-REGULATION | PHENOTYPE | E-CADHERIN | MIR-200 FAMILY | REPRESSORS ZEB1 | CELL BIOLOGY | EPITHELIAL-MESENCHYMAL TRANSITION | BREAST-CANCER | COLORECTAL-CANCER | Receptors, Notch - metabolism | Humans | Receptors, Notch - genetics | Gene Knockdown Techniques | Intercellular Signaling Peptides and Proteins - physiology | DNA-Binding Proteins - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Neoplasms - genetics | Membrane Proteins - physiology | Serrate-Jagged Proteins | Base Sequence | Membrane Proteins - metabolism | Nuclear Proteins - genetics | Jagged-1 Protein | Calcium-Binding Proteins - metabolism | Transcription Factors - physiology | DNA-Binding Proteins - antagonists & inhibitors | Membrane Proteins - genetics | Cells, Cultured | Intercellular Signaling Peptides and Proteins - genetics | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Signal Transduction - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Models, Biological | Calcium-Binding Proteins - physiology | Homeodomain Proteins - antagonists & inhibitors | Nuclear Proteins - antagonists & inhibitors | Signal Transduction - physiology | MicroRNAs - genetics | Feedback, Physiological - physiology | MicroRNAs - physiology | Homeodomain Proteins - physiology | Calcium-Binding Proteins - genetics | Zinc Finger E-box-Binding Homeobox 1 | Proteins | Signal transduction | Cellular biology | Molecular biology | Gene expression | Cancer
Journal Article
Cancer research (Chicago, Ill.), ISSN 0008-5472, 06/2011, Volume 71, Issue 11, pp. 4028 - 4039
Journal Article
Molecular cell, ISSN 1097-2765, 2009, Volume 35, Issue 5, pp. 563 - 573
The target of rapamycin complex 1 (TORC1) is a central regulator of eukaryotic cell growth that is activated by a variety of hormones (e.g., insulin) and... 
CELLBIO | PROTEINS | SIGNALING | YEAST SACCHAROMYCES-CEREVISIAE | CELL-GROWTH CONTROL | SIGNALING PATHWAYS | FUNCTIONAL HOMOLOG | RAG GTPASES | VACUOLE FUSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | AMINO-ACID PERMEASE | COMPONENT | GTP-BINDING PROTEINS | GAP1 PERMEASE | CELL BIOLOGY | Vacuoles - enzymology | Intracellular Membranes - enzymology | Saccharomyces cerevisiae - genetics | Multiprotein Complexes | Adaptor Proteins, Vesicular Transport - genetics | Saccharomyces cerevisiae - drug effects | Guanosine Triphosphate - metabolism | Adaptor Proteins, Vesicular Transport - metabolism | Vacuoles - drug effects | DNA-Binding Proteins - metabolism | Amino Acids - metabolism | Time Factors | Guanine Nucleotide Exchange Factors - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Guanosine Diphosphate - metabolism | Protein Synthesis Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Guanine Nucleotide Exchange Factors - genetics | Signal Transduction | Saccharomyces cerevisiae Proteins - antagonists & inhibitors | Monomeric GTP-Binding Proteins - genetics | Saccharomyces cerevisiae Proteins - genetics | Amino Acid Transport Systems - metabolism | Sirolimus - pharmacology | Cycloheximide - pharmacology | Protein Transport | Transcription Factors - metabolism | Monomeric GTP-Binding Proteins - metabolism | Saccharomyces cerevisiae Proteins - metabolism | Protein Binding | Saccharomyces cerevisiae - enzymology | Endosomes - enzymology | Intracellular Membranes - drug effects | Mutation | Saccharomyces cerevisiae - growth & development | Proteins | Purines | Amino acids | Gross domestic product | Guanosine
Journal Article
Oncogene, ISSN 0950-9232, 02/2008, Volume 27, Issue 7, pp. 997 - 1003
...Oncogene (2008) 27, 9971003 & 2008 Nature Publishing Group All rights reserved 0950-9232/08 $30.00 www.nature.com/onc ORIGINAL ARTICLE HDM2 antagonist Nutlin-3... 
HDM2 | Nutlin | p73 | Apoptosis | p53 | SITE | BIOCHEMISTRY & MOLECULAR BIOLOGY | apoptosis | MOLECULE MDM2 ANTAGONISTS | P53 PATHWAY | P63 | FAMILY | CELL BIOLOGY | ONCOLOGY | IN-VIVO | GENETICS & HEREDITY | SQUAMOUS-CELL CARCINOMA | MUTANT P53 | CENTRAL DOMAIN | Protein Biosynthesis | Immunoprecipitation | Humans | HCT116 Cells - metabolism | Immunoblotting | Bone Neoplasms - pathology | Tumor Suppressor Protein p53 - genetics | Bone Neoplasms - metabolism | DNA-Binding Proteins - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Transcription, Genetic | Bone Neoplasms - genetics | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors | Osteosarcoma - metabolism | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | RNA, Small Interfering - pharmacology | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Imidazoles - pharmacology | DNA-Binding Proteins - genetics | Nuclear Proteins - chemistry | DNA-Binding Proteins - chemistry | Piperazines - pharmacology | Apoptosis Regulatory Proteins - metabolism | HCT116 Cells - pathology | Protein Binding | Apoptosis - physiology | Osteosarcoma - genetics | Causes of | Tumor suppressor genes | Genetic aspects | Research | Health aspects | Cancer | Oncology | Genetics |