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Nature Communications, ISSN 2041-1723, 2012, Volume 3, Issue 1, p. 1208
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2008, Volume 105, Issue 12, pp. 4826 - 4831
To enhance therapeutic efficacy and reduce adverse effects, practitioners of traditional Chinese medicine (TCM) prescribe a combination of plant... 
Up regulation | Acute promyelocytic leukemia | Arsenic | Medical treatment | Leukemia | Cell cycle | Cell lines | Mice | Cellular differentiation | Blood | Traditional Chinese medicine | Active ingredient | Systems biology | Synergism | Tetraarsenic tetrasulfide | systems biology | NB4 | APOPTOSIS | PHOSPHORYLATION | active ingredient | MULTIDISCIPLINARY SCIENCES | tetraarsenic tetrasulfide | traditional chinese medicine | ARSENIC TRIOXIDE AS2O3 | IN-VITRO | RETINOIC ACID | THERAPY | GENE | synergism | CELL-CYCLE | EXPRESSION | Transcription, Genetic - drug effects | Oncogene Proteins, Fusion - metabolism | Leukemia, Promyelocytic, Acute - pathology | Humans | Drugs, Chinese Herbal - pharmacology | G1 Phase - drug effects | Aquaporins - genetics | Arsenicals - therapeutic use | Ubiquitination - drug effects | Protein Processing, Post-Translational - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Drugs, Chinese Herbal - therapeutic use | Disease Models, Animal | Sulfides - pharmacology | Medicine, Chinese Traditional | Arsenicals - pharmacology | Aquaporins - metabolism | Sulfides - therapeutic use | Drug Synergism | Up-Regulation - drug effects | Animals | Cell Differentiation - drug effects | Cell Line, Tumor | Resting Phase, Cell Cycle - drug effects | Leukemia, Promyelocytic, Acute - genetics | Leukemia, Promyelocytic, Acute - drug therapy | Evaluation | Medicine, Chinese | Research | Drug synergism | Index Medicus | Biological Sciences
Journal Article
Nature Medicine, ISSN 1078-8956, 09/2017, Volume 23, Issue 9, pp. 1055 - 1062
Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising anticancer therapies. The gene encoding the E3 ubiquitin ligase... 
SELECTIVE-INHIBITION | TARGET | MEDICINE, RESEARCH & EXPERIMENTAL | ANDROGEN RECEPTOR | STEM-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACUTE MYELOID-LEUKEMIA | ENHANCERS | CELL BIOLOGY | RNA-SEQ | BROMODOMAIN INHIBITION | MUTATIONS | BRD4 | Prostatic Neoplasms - metabolism | Immunoprecipitation | TOR Serine-Threonine Kinases - metabolism | Humans | Drug Resistance, Neoplasm | Male | Gene Expression Profiling | Molecular Targeted Therapy | Mechanistic Target of Rapamycin Complex 1 | Transcription Factors - drug effects | Multiprotein Complexes - metabolism | Prostatic Neoplasms - genetics | Proteasome Endopeptidase Complex - drug effects | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Nuclear Proteins - drug effects | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | TOR Serine-Threonine Kinases - drug effects | Multiprotein Complexes - drug effects | Prostatic Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | RNA-Binding Proteins - antagonists & inhibitors | Triazoles - therapeutic use | Cell Survival | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Azepines - therapeutic use | RNA-Binding Proteins - drug effects | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Nuclear Proteins - antagonists & inhibitors | Protein-Serine-Threonine Kinases - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mutation | RNA-Binding Proteins - metabolism | rac1 GTP-Binding Protein - metabolism | Proto-Oncogene Proteins c-akt - drug effects | rac1 GTP-Binding Protein - genetics | Gene mutations | Physiological aspects | Genetic aspects | Research | Drug resistance | Drug therapy | Prostate cancer | Ubiquitin | Inhibitor drugs | Stabilization | AKT protein | Activation | Biosynthesis | Degradation | Proteins | Ubiquitination | Transcription activation | Bioindicators | Ubiquitin-protein ligase | Binding | Rac1 protein | Tumor cell lines | Gene expression | Cholesterol | Mutants | Inhibitors | Proteasomes | Biomarkers | Bet protein | Prostate | Cancer | Guanosinetriphosphatase
Journal Article
Nature Cell Biology, ISSN 1465-7392, 02/2015, Volume 17, Issue 2, pp. 160 - 169
Journal Article
Journal Article
Journal of Cell Biology, ISSN 0021-9525, 2013, Volume 202, Issue 5, pp. 747 - 763
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 513, Issue 7516, pp. 95 - 99
Receptor interacting protein kinase 1 (RIPK1) has an essential role in the signalling triggered by death receptors and pattern recognition receptors(1,2).... 
UBIQUITINATION | NECROPTOSIS | MEDIATED RECOMBINATION | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | KINASE | MICE | TNF-ALPHA | CRE-LOXP | NECROSIS-FACTOR RECEPTOR-1 | CELL-DEATH | Intestines - drug effects | Protein Kinases - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Inflammation - pathology | Epithelial Cells - metabolism | Apoptosis - drug effects | Epithelial Cells - drug effects | Caspase 8 - metabolism | Male | NF-kappa B - metabolism | Intestines - metabolism | Organoids - enzymology | Necrosis | Caspase 8 - genetics | Receptors, Tumor Necrosis Factor, Type I - deficiency | Inflammation - metabolism | Gene Deletion | Organoids - metabolism | Female | Homeostasis - drug effects | Epithelial Cells - cytology | Tumor Necrosis Factors - pharmacology | Cell Survival - drug effects | Epithelium - drug effects | Epithelium - pathology | Intestines - pathology | Epithelium - metabolism | Organoids - cytology | Epithelial Cells - pathology | Mice, Knockout | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | Myeloid Differentiation Factor 88 - deficiency | Organoids - drug effects | Survival Analysis | Anti-Bacterial Agents - pharmacology | Mice | Receptor-Interacting Protein Serine-Threonine Kinases - deficiency | Intestines - cytology | Protein research | Physiological aspects | Homeostasis | Research | Epithelium | Protein kinases | Apoptosis | Proteins | Genotype & phenotype | Antibiotics | Transgenic animals | Rodents | Ligands | Colon | Kinases
Journal Article
Nature Medicine, ISSN 1078-8956, 05/2017, Volume 23, Issue 5, pp. 590 - 600
Journal Article
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 4728 - 16
PI3K/Akt signaling is activated in cancers and governs tumor initiation and progression, but how Akt is activated under diverse stresses is poorly understood.... 
OXIDATIVE STRESS | ENERGY STRESS | PHOSPHORYLATION | PROTEIN-KINASE | MULTIDISCIPLINARY SCIENCES | GROWTH-FACTOR | GLUCOSE DEPRIVATION | CELL-SURVIVAL | CANCER PROGRESSION | PC12 CELLS | HYPOXIA | Human Umbilical Vein Endothelial Cells - metabolism | Calcium - metabolism | Humans | Carcinogenesis - metabolism | Glycolysis - drug effects | Neovascularization, Pathologic - pathology | Ubiquitination - drug effects | Adenylate Kinase - metabolism | Stress, Physiological - drug effects | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Fibroblasts - metabolism | Cell Survival - drug effects | ErbB Receptors - metabolism | Enzyme Activation - drug effects | Phosphoserine - metabolism | S-Phase Kinase-Associated Proteins - metabolism | Disease Progression | Carcinogenesis - drug effects | Carcinogenesis - pathology | Cell Movement - drug effects | Animals | Signal Transduction - drug effects | Fibroblasts - drug effects | Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism | Cell Line, Tumor | Mice | Epidermal Growth Factor - pharmacology | Drug Resistance, Neoplasm - drug effects | Stresses | Phosphorylation | Animal models | Cell survival | AKT protein | Activation | Breast cancer | Glucose | Drug resistance | 1-Phosphatidylinositol 3-kinase | Ubiquitination | Epidermal growth factor | Skp2 protein | Calcium-binding protein | Tumorigenesis | Growth factors | Calmodulin | Ubiquitin-protein ligase | Calcium ions | Cancer | Tumors
Journal Article
Nature Medicine, ISSN 1078-8956, 01/2016, Volume 22, Issue 1, pp. 46 - 53
The ubiquitin proteasome system (UPS) degrades misfolded proteins including those implicated in neurodegenerative diseases. We investigated the effects of tau... 
SYSTEM | MEDICINE, RESEARCH & EXPERIMENTAL | KINASE-A | PHOSPHORYLATION | HELICAL FILAMENT-TAU | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | UBIQUITINATED PROTEINS ACTIVATE | CELL BIOLOGY | MOUSE MODEL | DEGRADATION | AGGREGATION | TRANSGENIC MICE | Immunoprecipitation | Native Polyacrylamide Gel Electrophoresis | Humans | tau Proteins - metabolism | Cognition Disorders - metabolism | Immunoblotting | Brain - metabolism | Ubiquitination | Proteasome Endopeptidase Complex - drug effects | HEK293 Cells | Behavior, Animal - drug effects | Rolipram - pharmacology | Cyclic AMP - metabolism | Cyclic AMP-Dependent Protein Kinases - drug effects | Disease Models, Animal | Cyclic AMP-Dependent Protein Kinases - metabolism | Mice, Transgenic | Cognition - drug effects | Phosphodiesterase 4 Inhibitors - pharmacology | Brain - drug effects | Tauopathies - metabolism | Animals | Signal Transduction - drug effects | Fluorescent Antibody Technique | Brain - pathology | Mice | Proteasome Endopeptidase Complex - metabolism | In Vitro Techniques | Protein Aggregation, Pathological - metabolism | Prevention | Physiological aspects | Genetic aspects | Cellular signal transduction | Cognition disorders | Research | Ubiquitin-proteasome system | Phosphorylation | Cognition & reasoning | Kinases | Proteases | Protein folding | Neurological disorders
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 1/2011, Volume 108, Issue 4, pp. 1433 - 1438
The major obstacle in cancer treatment is the resistance of cancer cells to therapies. Nrf2 is a transcription factor that regulates a cellular defense... 
Cell growth | Chemotherapy | Cell death | Cell lines | HeLa cells | Sensitization | Heterologous transplantation | Tumors | Lung neoplasms | Cancer | Reactive oxygen species | Antioxidant response | Chemosensitization | Natural compounds | CANCER-CELLS | natural compounds | INCREASED EXPRESSION | MULTIDISCIPLINARY SCIENCES | chemosensitization | ANTI-TUMOR AGENTS | KEAP1 | antioxidant response | BRUCEOSIDE-A | LUNG-CANCER | NRF2 | CUL3-BASED E3 LIGASE | reactive oxygen species | SQUAMOUS-CELL CARCINOMAS | SUBSTRATE ADAPTER PROTEIN | Lung Neoplasms - drug therapy | Apoptosis - drug effects | Glutathione - metabolism | Humans | Lung Neoplasms - metabolism | Immunoblotting | Lung Neoplasms - pathology | Antineoplastic Agents - administration & dosage | Cisplatin - administration & dosage | Quassins - pharmacology | Quassins - chemistry | Ubiquitination - drug effects | Antineoplastic Agents - pharmacology | Molecular Structure | Intracellular Space - drug effects | Quassins - administration & dosage | Cisplatin - pharmacology | Drug Synergism | Xenograft Model Antitumor Assays | Animals | Signal Transduction - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Mice, Nude | Intracellular Space - metabolism | NF-E2-Related Factor 2 - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | HeLa Cells | Physiological aspects | Drug resistance | Patient outcomes | Biological Sciences
Journal Article