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British journal of clinical pharmacology, ISSN 0306-5251, 2016, Volume 82, Issue 4, pp. 943 - 956
Journal Article
Biochemical journal, ISSN 1470-8728, 1998, Volume 335, Issue 1, pp. 1 - 13
.... How these molecules transduced the effects of agonists of PI-3K was unclear until the recent discovery that several protein kinases become activated upon exposure to 3... 
3T3-L1 ADIPOCYTES | SIGNAL-TRANSDUCTION | MYC-INDUCED APOPTOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | GLYCOGEN-SYNTHASE KINASE-3 | PLECKSTRIN HOMOLOGY DOMAIN | MOLECULAR-CLONING | GLUCOSE-TRANSPORT | GROWTH-FACTOR | PHOSPHOINOSITIDE 3-KINASE | P70 S6 KINASE
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
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2008, Volume 105, Issue 48, pp. 18782 - 18787
Journal Article
Leukemia, ISSN 0887-6924, 07/2011, Volume 25, Issue 7, pp. 1064 - 1079
It has become apparent that regulation of protein translation is an important determinant in controlling cell growth and leukemic transformation... 
mTOR | translation | sensitivity | PI3K | therapy | resistance | TUMOR-SUPPRESSOR CANDIDATE | PROTEIN-KINASE | INITIATION-FACTOR 4E | ACUTE MYELOID-LEUKEMIA | GROWTH-FACTOR RECEPTOR | BONE-MARROW MICROENVIRONMENT | ONCOLOGY | AKT/PROTEIN-KINASE-B | ACUTE LYMPHOBLASTIC-LEUKEMIA | HEMATOPOIETIC STEM-CELLS | CHRONIC LYMPHOCYTIC-LEUKEMIA | HEMATOLOGY | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Humans | Neoplasm Proteins - physiology | PTEN Phosphohydrolase - physiology | Apoptosis - genetics | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - genetics | Gene Expression Regulation, Leukemic - genetics | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | Transcription Factors - drug effects | TOR Serine-Threonine Kinases - antagonists & inhibitors | PTEN Phosphohydrolase - antagonists & inhibitors | TOR Serine-Threonine Kinases - genetics | Protein Processing, Post-Translational - drug effects | Drug Design | TOR Serine-Threonine Kinases - physiology | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | Neoplasm Proteins - genetics | Leukemia - genetics | Multiprotein Complexes - drug effects | PTEN Phosphohydrolase - genetics | Proteins - physiology | Transcription Factors - physiology | RNA, Messenger - genetics | Gene Expression Regulation, Leukemic - drug effects | Leukemia - drug therapy | Transcription Factors - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - physiology | Multiprotein Complexes - physiology | Phosphatidylinositol 3-Kinases - genetics | Drug Resistance, Neoplasm - genetics | Pseudogenes | Signal Transduction - drug effects | Phosphatidylinositol 3-Kinases - physiology | Proteins - drug effects | RNA, Neoplasm - genetics | Protein Biosynthesis - drug effects | MicroRNAs - genetics | Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects | Antimitotic agents | Genes | Leukemia | Physiological aspects | Development and progression | Genetic aspects | Research | Antineoplastic agents | Drug therapy | Health aspects
Journal Article
Cell Cycle, ISSN 1551-4005, 2014, Volume 8, Issue 16, pp. 2502 - 2508
The Akt (PKB) protein kinases are critical regulators of human physiology that control an impressive array of diverse cellular functions, including the modulation of growth, survival, proliferation and metabolism... 
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Glucose homeostasis | Akt2 | Isoforms | Akt1 | Akt | GLUT4 | Metabolism | Cellular growth | Signaling specificity | signaling specificity | GLUT4-CONTAINING VESICLES | STIMULATED GLUT4 TRANSLOCATION | GTPASE-ACTIVATING-PROTEIN | isoforms | PLASMA-MEMBRANE | MICE LACKING | CELL BIOLOGY | cellular growth | glucose homeostasis | SKELETAL-MUSCLE | GLUCOSE-HOMEOSTASIS | SIGNALING PATHWAY | CELL-MIGRATION | INSULIN-RESISTANCE | metabolism | cancer
Journal Article
Journal Article
Journal Article
Autophagy, ISSN 1554-8635, 2014, Volume 6, Issue 2, pp. 239 - 247