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British journal of clinical pharmacology, ISSN 0306-5251, 2016, Volume 82, Issue 4, pp. 943 - 956
Journal Article
Nature (London), ISSN 1476-4687, 2018, Volume 562, Issue 7725, pp. 69 - 75
Primary liver cancer represents a major health problem. It comprises hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), which differ... 
PATHOGENESIS | HEPATOCELLULAR-CARCINOMA | READ ALIGNMENT | HEPATOCYTES | DNA | INFLAMMATION | PACKAGE | MULTIDISCIPLINARY SCIENCES | FRAMEWORK | BINDING | DISCOVERY | Humans | Tumor Microenvironment | Apoptosis - genetics | Hepatocytes - pathology | Male | Gene Expression Profiling | Genes, myc | Hepatocytes - metabolism | Proto-Oncogene Proteins c-akt - genetics | DNA-Binding Proteins - metabolism | Carcinoma, Hepatocellular - genetics | DNA Transposable Elements - genetics | Female | Liver Neoplasms - pathology | Cell Differentiation | Cell Lineage - genetics | Disease Models, Animal | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | Cytokines - metabolism | Liver Neoplasms - genetics | Carcinogenesis - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Transcription Factors - metabolism | Cholangiocarcinoma - pathology | Animals | Epigenesis, Genetic - genetics | Carcinoma, Hepatocellular - pathology | Cholangiocarcinoma - genetics | Mosaicism | Mice | Necrosis - genetics | Genes, ras | Liver cancer | Research | Carcinogenesis | Oncology, Experimental | Apoptosis | Cancer | Animal models | Cytokines | Liver | Hepatocellular carcinoma | Genomes | Metastasis | Risk analysis | Gene expression | Risk factors | Metastases | Hepatocytes | Morphology | DNA methylation | Tumorigenesis | Bioinformatics | Cholangiocarcinoma | Deoxyribonucleic acid--DNA | Tumors | T-Box Domain Proteins/metabolism | Hepatocytes/pathology | DNA-Binding Proteins/metabolism | Life Sciences | Cholangiocarcinoma/pathology | Transcription Factors/metabolism | Necrosis/genetics | Cytokines/metabolism | Epigenesis, Genetic/genetics | Cyclin-Dependent Kinase Inhibitor p16/deficiency | Carcinoma, Hepatocellular/pathology | DNA Transposable Elements/genetics | Cell Lineage/genetics | T-Box Domain Proteins/genetics | Transcription Factors/genetics | Apoptosis/genetics | Proto-Oncogene Proteins c-akt/genetics | Liver Neoplasms/genetics | Cholangiocarcinoma/genetics | Liver Neoplasms/pathology | DNA-Binding Proteins/genetics | Hepatocytes/metabolism | Carcinoma, Hepatocellular/genetics | Carcinogenesis/genetics
Journal Article
PLoS biology, ISSN 1545-7885, 2009, Volume 7, Issue 6, p. e1000121
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
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2008, Volume 105, Issue 48, pp. 18782 - 18787
Journal Article
PloS one, ISSN 1932-6203, 2015, Volume 10, Issue 5, p. e0127942
Myocardial ischemia reperfusion injury (IRI) adversely affects cardiac performance and the prognosis of patients with acute myocardial infarction. Although... 
HEART | OVEREXPRESSION | HYPERTROPHY | JAK-STAT PATHWAY | MULTIDISCIPLINARY SCIENCES | KINASE | TRANSDUCER | INDUCIBLE GENE | TRANSCRIPTION-3 | AKT | CONFERS RESISTANCE | Mitogen-Activated Protein Kinase 3 - genetics | Myeloid Cell Leukemia Sequence 1 Protein - metabolism | Suppressor of Cytokine Signaling Proteins - genetics | Myocardium - pathology | Myeloid Cell Leukemia Sequence 1 Protein - genetics | Proto-Oncogene Proteins c-akt - genetics | MAP Kinase Signaling System | Mice, Knockout | Muscle Proteins - genetics | Myocardial Reperfusion Injury - metabolism | Suppressor of Cytokine Signaling 3 Protein | Phosphorylation - genetics | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Gene Deletion | Myocardium - metabolism | Muscle Proteins - metabolism | Mice | Suppressor of Cytokine Signaling Proteins - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Myocardial Reperfusion Injury - genetics | Myocardial Reperfusion Injury - prevention & control | Prevention | Physiological aspects | Cellular signal transduction | Research | Cytokines | Reperfusion injury | Heart | Myocardial infarction | Phosphorylation | Bcl-2 protein | Transcription | Physicians | Leukemia | Myocardial ischemia | AKT protein | Activation | Kinases | Proteins | Signal transduction | Mitochondria | Negative feedback | Reperfusion | Ischemia | Clonal deletion | Rodents | Janus kinase | Heart diseases | Internal medicine | Coronary artery | Stat3 protein | Extracellular signal-regulated kinase | Cardiomyocytes | Mcl-1 protein | Medicine | Signaling | Injury prevention | Coronary vessels | Infarction | Apoptosis
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