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1. Full Text Transcription Factor Foxo1 Represses T-bet-Mediated Effector Functions and Promotes Memory CD8+ T Cell Differentiation
by Rao, Rajesh R and Li, Qingsheng and Bupp, Melanie R. Gubbels and Shrikant, Protul A
Immunity, ISSN 1074-7613, 03/2012, Volume 36, Issue 3, pp. 374 - 387
The evolutionary conserved Foxo transcription factors are important regulators of quiescence and longevity. Although, Foxo1 is known to be important in... 
ACTIVATION | HOMEOSTASIS | MTORC2 | METABOLISM | KINASE | GROWTH | EOMESODERMIN | PROLIFERATION | IMMUNOLOGY | EXPRESSION | RIBOSOME | Forkhead Transcription Factors - immunology | CD8-Positive T-Lymphocytes - cytology | Multiprotein Complexes | T-Box Domain Proteins - immunology | Mechanistic Target of Rapamycin Complex 1 | CD8-Positive T-Lymphocytes - metabolism | Forkhead Transcription Factors - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - metabolism | Interleukin-12 - pharmacology | Mice, Inbred C57BL | Mice, Transgenic | Forkhead Transcription Factors - genetics | Sirolimus - pharmacology | Mice, Knockout | Cell Differentiation - immunology | Animals | Proteins - metabolism | CD8-Positive T-Lymphocytes - drug effects | Immunologic Memory | Trans-Activators - metabolism | Forkhead Box Protein O1 | Mice | TOR Serine-Threonine Kinases | Transcription Factors | CD8-Positive T-Lymphocytes - immunology | Proteins - antagonists & inhibitors | Proteins | Flow cytometry | Genotype & phenotype | Phosphorylation | Transcription factors | Statistical analysis | Kinases | Mammals | Index Medicus | IFN-γ | Akt | Eomesodermin | mTORC2 | IL-12 | CD8+ T cell | mTORC1 | T-bet | effector and memory differentiation | instructional programming | Foxo1
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2. Full Text AKT Inhibition Relieves Feedback Suppression of Receptor Tyrosine Kinase Expression and Activity
by Chandarlapaty, Sarat and Sawai, Ayana and Scaltriti, Maurizio and Rodrik-Outmezguine, Vanessa and Grbovic-Huezo, Olivera and Serra, Violeta and Majumder, Pradip K and Baselga, Jose and Rosen, Neal
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
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3. Full Text MicroRNA-9 regulates neurogenesis in mouse telencephalon by targeting multiple transcription factors
by Shibata, Mikihito and Nakao, Hiromi and Kiyonari, Hiroshi and Abe, Takaya and Aizawa, Shinichi
Journal of Neuroscience, ISSN 0270-6474, 03/2011, Volume 31, Issue 9, pp. 3407 - 3422
microRNA-9-2 and microRNA-9-3 double-mutant mice demonstrate that microRNA-9 (miR-9) controls neural progenitor proliferation and differentiation in the... 
CORTICAL INTERNEURONS | GANGLIONIC EMINENCE | TRANSLATIONAL REPRESSION | STEM-CELL | NEURONAL DIFFERENTIATION | SUBVENTRICULAR ZONE | MIDBRAIN-HINDBRAIN BOUNDARY | HUNTINGTONS-DISEASE | NEUROSCIENCES | INTERMEDIATE PROGENITOR CELLS | MOLECULAR-MECHANISMS | Gene Targeting - methods | Receptors, Cytoplasmic and Nuclear - deficiency | Humans | Nerve Tissue Proteins - deficiency | Transcription Factors - deficiency | Receptors, Cytoplasmic and Nuclear - biosynthesis | Neurogenesis - genetics | Neurons - physiology | Female | Forkhead Transcription Factors - antagonists & inhibitors | Forkhead Transcription Factors - deficiency | Nerve Tissue Proteins - antagonists & inhibitors | Homeodomain Proteins - biosynthesis | Mice, Inbred C57BL | Cells, Cultured | Mice, Transgenic | Up-Regulation - genetics | Receptors, Cytoplasmic and Nuclear - genetics | Telencephalon - embryology | Transcription Factors - genetics | Forkhead Transcription Factors - genetics | Nerve Tissue Proteins - genetics | Down-Regulation - genetics | Homeodomain Proteins - genetics | Pregnancy | Transcription Factors - metabolism | Telencephalon - physiology | Animals | Neurogenesis - physiology | Mice | MicroRNAs - genetics | MicroRNAs - physiology | Index Medicus
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4. Full Text Direct and Indirect Gene Regulation by a Life-Extending FOXO Protein in C. elegans: Roles for GATA Factors and Lipid Gene Regulators
by Zhang, Peichuan and Judy, Meredith and Lee, Seung-Jae and Kenyon, Cynthia
Cell Metabolism, ISSN 1550-4131, 01/2013, Volume 17, Issue 1, pp. 85 - 100
In long-lived insulin/IGF-1 pathway mutants, the life-extending FOXO transcription factor DAF-16 is present throughout the animal, but we find that its... 
FAT-BODY | LONGEVITY | INSULIN-RECEPTOR | CAENORHABDITIS-ELEGANS | SIGNALING PATHWAY | DAF-16 | ENDOCRINOLOGY & METABOLISM | BETA-AMYLOID PEPTIDE | TRANSCRIPTION FACTOR | EXPRESSION | SPAN EXTENSION | CELL BIOLOGY | Promoter Regions, Genetic | Caenorhabditis elegans - metabolism | Gene Expression Regulation | Caenorhabditis elegans Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Longevity | Transcription Factors - genetics | GATA Transcription Factors - genetics | Receptor, Insulin - antagonists & inhibitors | Endoderm - metabolism | Transcription Factors - metabolism | Animals | Caenorhabditis elegans Proteins - antagonists & inhibitors | GATA Transcription Factors - metabolism | RNA Interference | Receptor, Insulin - genetics | Amyloid beta-Peptides - metabolism | Aging | Protein Binding | Receptor, Insulin - metabolism | Mutation | Caenorhabditis elegans Proteins - genetics | Forkhead Transcription Factors | RNA, Small Interfering - metabolism | Caenorhabditis elegans | Gene expression | Alzheimer's disease | Analysis | Index Medicus
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5. Full Text The HSP90 inhibitor XL888 overcomes BRAF inhibitor resistance mediated through diverse mechanisms
by Paraiso, Kim H.T and Haarberg, H. Eirik and Wood, Elizabeth and Rebecca, Vito W and Chen, Y. Ann and Xiang, Yun and Ribas, Antoni and Lo, Roger S and Weber, Jeffrey S and Sondak, Vernon K and John, Jobin K and Sarnaik, Amod A and Koomen, John M and Smalley, Keiran S.M
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
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6. Full Text Glycolysis controls the induction of human regulatory T cells by modulating the expression of FOXP3 exon 2 splicing variants
by De Rosa, Veronica and Galgani, Mario and Porcellini, Antonio and Colamatteo, Alessandra and Santopaolo, Marianna and Zuchegna, Candida and Romano, Antonella and De Simone, Salvatore and Procaccini, Claudio and La Rocca, Claudia and Carrieri, Pietro Biagio and Maniscalco, Giorgia Teresa and Salvetti, Marco and Buscarinu, Maria Chiara and Franzese, Adriana and Mozzillo, Enza and La Cava, Antonio and Matarese, Giuseppe
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
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7. Full Text ROS inhibitor N-acetyl-L-cysteine antagonizes the activity of proteasome inhibitors
by Halasi, Marianna and Wang, Ming and Chavan, Tanmay S and Gaponenko, Vadim and Hay, Nissim and Gartel, Andrei L
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)
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8. Full Text The SKN‐1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms
by Tullet, Jennifer M.A and Green, James W and Au, Catherine and Benedetto, Alexandre and Thompson, Maximillian A and Clark, Emily and Gilliat, Ann F and Young, Adelaide and Schmeisser, Kathrin and Gems, David
Aging Cell, ISSN 1474-9718, 10/2017, Volume 16, Issue 5, pp. 1191 - 1194
In C. elegans, the skn‐1 gene encodes a transcription factor that resembles mammalian Nrf2 and activates a detoxification response. skn‐1 promotes resistance... 
transcription regulation | C. elegans | aging | oxidative stress | LONGEVITY | CAENORHABDITIS-ELEGANS | GENETICS | DAF-16 | CELL BIOLOGY | GERIATRICS & GERONTOLOGY | Caenorhabditis elegans - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Caenorhabditis elegans - growth & development | Oxidative Stress | Signal Transduction | Caenorhabditis elegans - genetics | Caenorhabditis elegans Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Longevity - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Forkhead Transcription Factors - genetics | DNA-Binding Proteins - metabolism | Transcription Factors - metabolism | Animals | Caenorhabditis elegans Proteins - antagonists & inhibitors | RNA Interference | Forkhead Transcription Factors - metabolism | Gene Expression Regulation, Developmental | Caenorhabditis elegans Proteins - genetics | Physiological aspects | Oxidative stress | Index Medicus | Short Takes | Short Take
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9. Full Text Glucose Shortens the Life Span of C. elegans by Downregulating DAF-16/FOXO Activity and Aquaporin Gene Expression
by Lee, Seung-Jae and Murphy, Coleen T and Kenyon, Cynthia
Cell Metabolism, ISSN 1550-4131, 2009, Volume 10, Issue 5, pp. 379 - 391
Many studies have addressed the effect of dietary glycemic index on obesity and diabetes, but little is known about its effect on life span itself. We found... 
HUMDISEASE | INSULIN | GLYCEMIC INDEX | OXIDATIVE STRESS | PROTEIN DAF-16 | GLYCEROL CHANNEL | HUMAN LONGEVITY | HEAT-SHOCK FACTOR | SIGNALING PATHWAY | ENDOCRINOLOGY & METABOLISM | NEMATODE CAENORHABDITIS-ELEGANS | STRESS RESISTANCE | CELL BIOLOGY | Caenorhabditis elegans Proteins - metabolism | Aquaporin 1 - metabolism | Heat Shock Transcription Factors | DNA-Binding Proteins - metabolism | Caenorhabditis elegans - physiology | Aquaporin 1 - antagonists & inhibitors | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | Down-Regulation | Transcription Factors - antagonists & inhibitors | Longevity | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Gene Knockout Techniques | Aquaporin 1 - genetics | Transcription Factors - metabolism | Feedback, Physiological | Insulin - metabolism | Animals | Caenorhabditis elegans Proteins - antagonists & inhibitors | Glycerol - metabolism | Receptor, IGF Type 1 - physiology | Glucose - metabolism | Caenorhabditis elegans Proteins - genetics | Forkhead Transcription Factors | Glycerin | Heat shock proteins | Glycerol | Glucose | Diabetes | Gene expression | Dextrose | Index Medicus
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10. Full Text The transcription factor FOXM1 is a cellular target of the natural product thiostrepton
by Hegde, Nagaratna S and Sanders, Deborah A and Rodriguez, Raphaël and Balasubramanian, Shankar
Nature Chemistry, ISSN 1755-4330, 09/2011, Volume 3, Issue 9, pp. 725 - 731
Transcription factors are proteins that bind specifically to defined DNA sequences to promote gene expression. Targeting transcription factors with small... 
BREAST-CANCER CELLS | BIOLOGY | SMALL ORGANIC-MOLECULES | ESTROGEN | INDUCE APOPTOSIS | MELANOMA-CELLS | PROTEASOME INHIBITORS | EXPRESSION | CHEMISTRY, MULTIDISCIPLINARY | PROGRESSION | DISCOVERY | Thiostrepton - pharmacology | Humans | Thiostrepton - analogs & derivatives | Anti-Bacterial Agents - metabolism | Biological Products - pharmacology | DNA - metabolism | Thiostrepton - metabolism | Biological Products - chemistry | Forkhead Transcription Factors - metabolism | Anti-Bacterial Agents - chemistry | Drug Design | Biological Products - metabolism | Cell Line, Tumor | Protein Binding | Cell Extracts | Anti-Bacterial Agents - pharmacology | Forkhead Transcription Factors - antagonists & inhibitors | Forkhead Box Protein M1 | Index Medicus
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11. Full Text FoxO3 Controls Autophagy in Skeletal Muscle In Vivo
by Mammucari, Cristina and Milan, Giulia and Romanello, Vanina and Masiero, Eva and Rudolf, Ruediger and Del Piccolo, Paola and Burden, Steven J and Di Lisi, Raffaella and Sandri, Marco and Sandri, Claudia and Zhao, Jinghui and Goldberg, Alfred L and Schiaffino, Stefano
Cell Metabolism, ISSN 1550-4131, 2007, Volume 6, Issue 6, pp. 458 - 471
Autophagy allows cell survival during starvation through the bulk degradation of proteins and organelles by lysosomal enzymes. However, the mechanisms... 
PROTEINS | HUMDISEASE | TRANSCRIPTION FACTORS | SIGNALING PATHWAY | PROTEIN BNIP3 | GROWTH | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | ATROPHY INVOLVE | MICE | ATROGIN-1 | HYPOXIA | UBIQUITIN LIGASES | CELL BIOLOGY | Protein Kinases - metabolism | Protein Kinases - genetics | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Ubiquitin - metabolism | Muscle, Skeletal - metabolism | Autophagy - physiology | Mitochondrial Proteins - genetics | Muscle, Skeletal - cytology | Proto-Oncogene Proteins c-akt - genetics | Lysosomes - metabolism | RNA Interference | Forkhead Transcription Factors - metabolism | Mitochondrial Proteins - metabolism | Membrane Proteins - metabolism | Autophagy - genetics | Forkhead Transcription Factors - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - metabolism | Muscular Atrophy - metabolism | Membrane Proteins - genetics | Muscular Atrophy - pathology | Gene Expression Regulation | Mice, Transgenic | Muscular Atrophy - genetics | Forkhead Transcription Factors - genetics | Animals | Models, Biological | Mice | TOR Serine-Threonine Kinases | Proteasome Endopeptidase Complex - metabolism | Forkhead Box Protein O3 | Ubiquitin | Muscles | Enzymes | Starvation | Genetic transcription | Proteolysis | Index Medicus
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12. Full Text FOXO3a regulates reactive oxygen metabolism by inhibiting mitochondrial gene expression
by Ferber, E.C and Peck, B and Delpuech, O and Bell, G.P and East, P and Schulze, A
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
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