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Immunity, ISSN 1074-7613, 03/2012, Volume 36, Issue 3, pp. 374 - 387
Journal Article
Cancer Cell, ISSN 1535-6108, 2011, Volume 19, Issue 1, pp. 58 - 71
Activation of the PI3K-AKT pathway in tumors is modulated by negative feedback, including mTORC1-mediated inhibition of upstream signaling. We now show that... 
RAPAMYCIN | TARGET | FORKHEAD TRANSCRIPTION FACTOR | CELLS | INSULIN-RECEPTOR | ACTIVATION | ONCOLOGY | SIGNALING PATHWAY | PHOSPHORYLATION | UPSTREAM | HUMAN CANCER | CELL BIOLOGY | RNA, Small Interfering - genetics | Receptor, IGF Type 1 - metabolism | Protein Binding - genetics | Receptor, ErbB-3 - metabolism | Humans | Forkhead Transcription Factors - metabolism | Protein Binding - drug effects | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Receptor, ErbB-2 - antagonists & inhibitors | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Quinoxalines - therapeutic use | Carcinoma, Non-Small-Cell Lung - metabolism | Receptor, ErbB-3 - genetics | Receptor Protein-Tyrosine Kinases - metabolism | Breast Neoplasms - drug therapy | Receptor, IGF Type 1 - genetics | Signal Transduction - drug effects | Mice, Nude | Models, Biological | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | Feedback, Physiological - physiology | Quinazolines - pharmacology | Proteins - antagonists & inhibitors | Neoplasms - metabolism | Gene Expression - drug effects | Multiprotein Complexes | Receptor, ErbB-2 - metabolism | Promoter Regions, Genetic - genetics | Proto-Oncogene Proteins c-akt - genetics | Breast Neoplasms - metabolism | Mechanistic Target of Rapamycin Complex 1 | Quinoxalines - pharmacology | Receptor, Insulin - genetics | Female | Forkhead Transcription Factors - antagonists & inhibitors | Gene Expression Regulation, Neoplastic - drug effects | Drug Therapy, Combination | Gene Expression Regulation, Neoplastic - physiology | Carcinoma, Non-Small-Cell Lung - pathology | Up-Regulation - genetics | Forkhead Transcription Factors - genetics | Xenograft Model Antitumor Assays | Animals | Receptor Protein-Tyrosine Kinases - genetics | Breast Neoplasms - pathology | Protein Kinase Inhibitors - therapeutic use | Quinazolines - therapeutic use | Feedback, Physiological - drug effects | Receptor, Insulin - metabolism | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Benzylamines - pharmacology | Benzylamines - therapeutic use | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 03/2011, Volume 31, Issue 9, pp. 3407 - 3422
Journal Article
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 05/2012, Volume 18, Issue 9, pp. 2502 - 2514
Purpose: The clinical use of BRAF inhibitors is being hampered by the acquisition of drug resistance. This study shows the potential therapeutic use of the... 
BREAST-CANCER | MULTIPLE-MYELOMA | APOPTOSIS | PHASE-II TRIAL | TANESPIMYCIN 17-AAG | TRASTUZUMAB | ONCOLOGY | BIM | ACQUIRED-RESISTANCE | MELANOMA-CELLS | POTENTIAL MECHANISM | Prospective Studies | Apoptosis - drug effects | Humans | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Immunoenzyme Techniques | Forkhead Transcription Factors - metabolism | Colony-Forming Units Assay | Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization | Phthalic Acids - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Real-Time Polymerase Chain Reaction | Proto-Oncogene Proteins B-raf - metabolism | Membrane Proteins - genetics | Melanoma - pathology | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Apoptosis Regulatory Proteins - metabolism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Indoles - adverse effects | Membrane Proteins - antagonists & inhibitors | Signal Transduction - drug effects | HSP90 Heat-Shock Proteins - antagonists & inhibitors | Cell Line, Tumor | HSP90 Heat-Shock Proteins - metabolism | Mice | Mice, Inbred BALB C | Forkhead Box Protein O3 | Azabicyclo Compounds - pharmacology | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | Proto-Oncogene Proteins c-bcl-2 - metabolism | Flow Cytometry | Bcl-2-Like Protein 11 | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | Forkhead Transcription Factors - antagonists & inhibitors | Melanoma - metabolism | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | RNA, Messenger - genetics | Proto-Oncogene Proteins - genetics | Forkhead Transcription Factors - genetics | Phosphatidylinositol 3-Kinases - genetics | Animals | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Myeloid Cell Leukemia Sequence 1 Protein | Apoptosis Regulatory Proteins - antagonists & inhibitors | Fluorescent Antibody Technique | Sulfonamides - adverse effects | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-bcl-2 - genetics | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects | Index Medicus
Journal Article
Nature Immunology, ISSN 1529-2908, 10/2015, Volume 16, Issue 11, pp. 1174 - 1184
Human regulatory T cells (T-reg cells) that develop from conventional T cells (T-conv cells) cells) following suboptimal stimulation via the T cell antigen... 
ACTIVATION | ALPHA-ENOLASE | TOLERANCE | IN-VIVO | EFFECTOR FUNCTION | EXPANSION | GENERATION | DIFFERENTIATION | IMMUNOLOGY | IDENTIFICATION | MTOR | Autoimmunity | T-Lymphocytes, Regulatory - metabolism | T-Lymphocytes, Regulatory - classification | Alternative Splicing | Tumor Suppressor Proteins - antagonists & inhibitors | Exons | Humans | Middle Aged | Male | Phosphopyruvate Hydratase - metabolism | CD4-Positive T-Lymphocytes - classification | RNA, Messenger - metabolism | Case-Control Studies | Gene Knockdown Techniques | T-Lymphocytes, Regulatory - immunology | CD4-Positive T-Lymphocytes - immunology | DNA-Binding Proteins - metabolism | Genetic Variation | Glycolysis - genetics | Young Adult | Signal Transduction - immunology | Phosphopyruvate Hydratase - genetics | Forkhead Transcription Factors - metabolism | Tumor Suppressor Proteins - genetics | Biomarkers, Tumor - metabolism | Adult | Female | Forkhead Transcription Factors - antagonists & inhibitors | Biomarkers, Tumor - antagonists & inhibitors | Fatty Acids - metabolism | Multiple Sclerosis, Relapsing-Remitting - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Multiple Sclerosis, Relapsing-Remitting - immunology | Oxidation-Reduction | Receptors, Antigen, T-Cell - metabolism | RNA, Messenger - genetics | CD4-Positive T-Lymphocytes - metabolism | Metabolome | Phosphopyruvate Hydratase - antagonists & inhibitors | DNA-Binding Proteins - genetics | Forkhead Transcription Factors - genetics | Multiple Sclerosis, Relapsing-Remitting - genetics | Biomarkers, Tumor - genetics | In Vitro Techniques | Physiological aspects | Glycolysis | Genetic aspects | Research | T cells | Index Medicus
Journal Article
Biochemical Journal, ISSN 0264-6021, 09/2013, Volume 454, Issue 2, pp. 201 - 208
NAC (N-acetyl-L-cysteine) is commonly used to identify and test ROS (reactive oxygen species) inducers, and to inhibit ROS. In the present study, we identified... 
Catalase | N-acetyl-L-cysteine (NAC) | Proteasome inhibitor | Reactive oxygen species (ROS) | Forkhead box protein M1 (FOXM1) | CANCER-CELLS | TARGET | APOPTOSIS | OXIDATIVE STRESS | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | reactive oxygen species (ROS) | ENDOPLASMIC-RETICULUM STRESS | BORTEZOMIB | FOXM1 | INACTIVATION | proteasome inhibitor | LACTACYSTIN | catalase | Free Radical Scavengers - pharmacology | Oxidants - pharmacology | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Humans | Acetylcysteine - metabolism | Proteasome Inhibitors - chemistry | Proteasome Inhibitors - metabolism | Viral Proteins - metabolism | Antineoplastic Agents, Phytogenic - antagonists & inhibitors | Chromans - metabolism | Proteasome Endopeptidase Complex - drug effects | Chromans - pharmacology | Dioxolanes - pharmacology | Forkhead Transcription Factors - metabolism | Forkhead Transcription Factors - antagonists & inhibitors | Ubiquitinated Proteins - metabolism | Recombinant Proteins - metabolism | Recombinant Proteins - antagonists & inhibitors | Free Radical Scavengers - metabolism | Proteasome Inhibitors - pharmacology | Catalase - genetics | Chromans - antagonists & inhibitors | Hydrogen Peroxide - pharmacology | Viral Proteins - genetics | Oxidants - antagonists & inhibitors | Dioxolanes - antagonists & inhibitors | Forkhead Transcription Factors - genetics | Catalase - metabolism | Reactive Oxygen Species - antagonists & inhibitors | Protein Stability - drug effects | Acetylcysteine - pharmacology | Cell Line, Tumor | Cytomegalovirus - enzymology | Proteasome Endopeptidase Complex - metabolism | Antineoplastic Agents, Phytogenic - pharmacology | Forkhead Box Protein M1 | Hydrogen Peroxide - antagonists & inhibitors | Index Medicus | N-acetyl-l-cysteine (NAC)
Journal Article
Journal Article
Journal Article
Cell Metabolism, ISSN 1550-4131, 2007, Volume 6, Issue 6, pp. 458 - 471
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 06/2012, Volume 19, Issue 6, pp. 968 - 979
Forkhead transcription factors of the O class (FOXOs) are important targets of the phosphatidylinositol 3-kinase/Akt pathway, and are key regulators of the... 
C-Myc | FOXO | Reactive oxygen species | HIF-1a | Mitochondrial biogenesis | TRANSFORMATION | FORKHEAD TRANSCRIPTION FACTOR | C-MYC DEGRADATION | ACTIVATION | HIF-1 alpha | PROTEIN-KINASE-B | c-Myc | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | HYPOXIA | mitochondrial biogenesis | CELL BIOLOGY | COMPLEX-III | BIOGENESIS | reactive oxygen species | ROS | Reactive Oxygen Species - metabolism | DNA, Mitochondrial - metabolism | Oxidative Stress | Signal Transduction | Humans | Gene Expression Regulation | Mitochondria - metabolism | Forkhead Transcription Factors - genetics | Proto-Oncogene Proteins c-myc - metabolism | Cell Hypoxia | Mitochondria - genetics | RNA Interference | Forkhead Transcription Factors - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Proto-Oncogene Proteins c-myc - antagonists & inhibitors | Cell Line, Tumor | Forkhead Box Protein O1 | Proto-Oncogene Proteins c-myc - genetics | Forkhead Transcription Factors - antagonists & inhibitors | Forkhead Box Protein O3 | Superoxide Dismutase - metabolism | Apoptosis | RNA, Small Interfering - metabolism | Index Medicus | Oxidative stress | Transcription factors | Hypoxia-inducible factor 1 alpha | Detoxification | c-Myc protein | AKT protein | Data processing | Superoxide dismutase | Mitochondrial DNA | Gene expression | Metabolism | Gene silencing | Mitochondria | Cell cycle | Forkhead protein | copy number | FOXO3 protein | Original Paper | HIF-1α
Journal Article