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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
Nature, ISSN 0028-0836, 07/2011, Volume 475, Issue 7354, pp. 106 - 110
Reactive oxygen species (ROS) are mutagenic and may thereby promote cancer(1). Normally, ROS levels are tightly controlled by an inducible antioxidant program... 
TRANSFORMATION | OXIDATIVE STRESS | ACTIVATION | INHIBITION | K-RAS | PATHWAY | MULTIDISCIPLINARY SCIENCES | PANCREATIC-CANCER | HEME OXYGENASE-1 | MUTATIONS | EXPRESSION | NIH 3T3 Cells | Cell Proliferation | Pancreatic Neoplasms - metabolism | Reactive Oxygen Species - metabolism | Cytoskeletal Proteins - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Antioxidants - metabolism | Humans | JNK Mitogen-Activated Protein Kinases - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | MAP Kinase Signaling System | Mitogen-Activated Protein Kinase Kinases - metabolism | Cell Transformation, Neoplastic - genetics | Cytoskeletal Proteins - metabolism | NF-E2-Related Factor 2 - genetics | Intracellular Signaling Peptides and Proteins - genetics | Kelch-Like ECH-Associated Protein 1 | Proto-Oncogene Proteins B-raf - metabolism | Fibroblasts - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Oncogenes - genetics | Oxidation-Reduction | Pancreatic Neoplasms - pathology | Cells, Cultured | Pancreatic Neoplasms - genetics | NF-E2-Related Factor 2 - deficiency | Cell Transformation, Neoplastic - metabolism | Animals | Proto-Oncogene Proteins B-raf - genetics | Genes, myc - genetics | NF-E2-Related Factor 2 - metabolism | Adaptor Proteins, Signal Transducing - genetics | Alleles | Cell Line, Tumor | Mice | Adaptor Proteins, Signal Transducing - metabolism | Cell Transformation, Neoplastic - pathology | Polymerase chain reaction | Usage | Reactive oxygen species | Physiological aspects | Research | Gene expression | Oncogenes | Studies | Mass spectrometry | Rodents | Evacuations & rescues | Cancer | Index Medicus
Journal Article
EMBO reports, ISSN 1469-221X, 01/2010, Volume 11, Issue 1, pp. 45 - 51
Autophagy is the cellular homeostatic pathway that delivers large cytosolic materials for degradation in the lysosome. Recent evidence indicates that autophagy... 
mitophagy | Nix | LC3 | GABARAP | selective autophagy | Selective autophagy | Mitophagy | APOPTOSIS | PROTEIN | RETICULOCYTE MATURATION | UBIQUITIN | BNIP3 | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-DEATH | CELL BIOLOGY | STRUCTURAL BASIS | DEGRADATION | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Humans | Cercopithecus aethiops | Molecular Sequence Data | Substrate Specificity | Autophagy - physiology | Mitochondrial Proteins - genetics | Proto-Oncogene Proteins - chemistry | Mitochondrial Proteins - metabolism | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Membrane Proteins - metabolism | Binding Sites | Proto-Oncogene Proteins - metabolism | Amino Acid Sequence | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cells, Cultured | Ubiquitin-Protein Ligases - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Saccharomyces cerevisiae Proteins - genetics | Blotting, Western | Amino Acid Motifs | Autophagy-Related Protein 8 Family | Animals | Membrane Proteins - chemistry | Reticulocytes - cytology | Mitochondrial Proteins - chemistry | Saccharomyces cerevisiae Proteins - metabolism | Protein Binding | Mice | Receptors, GABA-A - metabolism | COS Cells | Proteins | Mitochondria | Cellular biology | Cytoplasm | Index Medicus | Scientific Report
Journal Article
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 06/2009, Volume 296, Issue 6, pp. 1258 - 1270
Myostatin is a negative regulator of skeletal muscle size, previously shown to inhibit muscle cell differentiation. Myostatin requires both Smad2 and Smad3... 
MAFbx | Mammalian target of rapamycin complex signaling | MuRF1 | S6 kinase | Smad signaling | Human skeletal muscle cells | Transducer of regulated Ca | responsive element-binding protein activity | MuRF-1 | Atrogin | Transforming growth factor-β-like molecules | IGF-I | PHYSIOLOGY | ATROPHY | RAPID DISUSE | human skeletal muscle cells | transforming growth factor-beta-like molecules | SKELETAL-MUSCLE HYPERTROPHY | FOXO TRANSCRIPTION FACTORS | UBIQUITIN LIGASES | transducer of regulated Ca2+-responsive element-binding protein activity | CELL BIOLOGY | atrogin | PATHWAY | GROWTH | GENE-EXPRESSION | mammalian target of rapamycin complex signaling | CONDITIONAL ACTIVATION | Activin Receptors, Type I - antagonists & inhibitors | Protein Kinases - metabolism | Phosphorylation | Protein Kinases - genetics | Humans | Smad3 Protein - metabolism | Muscle Fibers, Skeletal - drug effects | Tripartite Motif Proteins | Smad3 Protein - genetics | Transfection | RNA Interference | Myoblasts, Skeletal - pathology | Smad2 Protein - genetics | Muscle Proteins - metabolism | Dioxoles - pharmacology | Regulatory-Associated Protein of mTOR | Benzamides - pharmacology | Myostatin - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Rapamycin-Insensitive Companion of mTOR Protein | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Signal Transduction | Cell Size - drug effects | Cells, Cultured | Smad2 Protein - metabolism | Ubiquitin-Protein Ligases - metabolism | Organ Size | Activin Receptors, Type I - metabolism | Myoblasts, Skeletal - enzymology | SKP Cullin F-Box Protein Ligases - metabolism | Mice, SCID | Myostatin - antagonists & inhibitors | Adaptor Proteins, Signal Transducing | Animals | Carrier Proteins - metabolism | Proteins - metabolism | Cell Differentiation - drug effects | Follistatin - pharmacology | Muscle Fibers, Skeletal - pathology | Creatine Kinase - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | TOR Serine-Threonine Kinases | Myoblasts, Skeletal - drug effects | Insulin-Like Growth Factor I - metabolism | Muscle Fibers, Skeletal - enzymology | RNA, Small Interfering - metabolism | Abdominal surgery | Musculoskeletal system | Signal transduction | Cell growth | Kinases | Gene expression | Cells | Index Medicus
Journal Article
Acta Physiologica, ISSN 1748-1708, 07/2013, Volume 208, Issue 3, pp. 251 - 264
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 12/2009, Volume 119, Issue 12, pp. 3626 - 3636
The polycomb group protein B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1) is dysregulated in various cancers, and its upregulation strongly correlates... 
MEDICINE, RESEARCH & EXPERIMENTAL | BREAST-CANCER CELLS | DEVELOPMENTAL REGULATORS | CELLULAR MEMORY | E-CADHERIN EXPRESSION | HEMATOPOIETIC STEM-CELLS | PROSTATE-CANCER | MYC TRANSGENIC MICE | SELF-RENEWAL | NF-KAPPA-B | TRANSCRIPTION FACTOR | Nasopharyngeal Neoplasms - genetics | Neoplasm Transplantation | Nasopharyngeal Neoplasms - metabolism | Epithelial Cells - metabolism | Cadherins - metabolism | Humans | Glycogen Synthase Kinase 3 beta | Transplantation, Heterologous | Phosphatidylinositol 3-Kinases - metabolism | Mesoderm - cytology | Repressor Proteins - antagonists & inhibitors | Nasopharyngeal Neoplasms - pathology | Cadherins - genetics | Epithelial Cells - cytology | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Nasopharyngeal Neoplasms - etiology | Snail Family Transcription Factors | Nasopharynx - metabolism | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | PTEN Phosphohydrolase - genetics | Proto-Oncogene Proteins - antagonists & inhibitors | Signal Transduction | Neoplasm Invasiveness | Down-Regulation | Gene Silencing | PTEN Phosphohydrolase - metabolism | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | Glycogen Synthase Kinase 3 - metabolism | Transcription Factors - metabolism | Animals | Polycomb Repressive Complex 1 | Mice, Nude | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Mesoderm - metabolism | Mice | Nasopharynx - cytology | Chromatin | Care and treatment | Lymphomas | Research | Analysis | Cancer | Index Medicus | Abridged Index Medicus
Journal Article
Oncogene, ISSN 0950-9232, 01/2016, Volume 35, Issue 1, pp. 12 - 21
Journal Article
Science, ISSN 0036-8075, 12/2010, Volume 330, Issue 6009, pp. 1390 - 1393
Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled. We provide in... 
T lymphocytes | Mitochondria | Cytokines | Thymocytes | Neurons | Cell death | REPORTS | Cytochromes | Mice | Potassium | Apoptosis | NEURONAL APOPTOSIS | CYTOCHROME-C | MITOCHONDRIAL APOPTOSIS | MECHANISM | MULTIDISCIPLINARY SCIENCES | BH3 DOMAINS | RELEASE | JNK PATHWAY | PROTEINS | BCL-2 FAMILY-MEMBERS | MEMBRANE PERMEABILIZATION | BH3 Interacting Domain Death Agonist Protein - deficiency | T-Lymphocytes - physiology | bcl-2-Associated X Protein - chemistry | Protein Multimerization | Stress, Physiological | bcl-2 Homologous Antagonist-Killer Protein - genetics | BH3 Interacting Domain Death Agonist Protein - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Membrane Proteins - deficiency | Caspases - metabolism | Bcl-2-Like Protein 11 | Apoptosis Regulatory Proteins - deficiency | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | Neurons - physiology | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | bcl-2-Associated X Protein - genetics | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cytochromes c - metabolism | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Permeability | Proto-Oncogene Proteins - deficiency | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Models, Biological | Cerebellum - cytology | Intracellular Membranes - metabolism | bcl-2 Homologous Antagonist-Killer Protein - chemistry | Protein research | Genetic aspects | Mitochondrial DNA | Biochemical genetics | Research | Properties | Methods | Index Medicus
Journal Article
Science, ISSN 0036-8075, 01/2014, Volume 343, Issue 6173, pp. 885 - 888
Journal Article