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Nature, ISSN 0028-0836, 05/2016, Volume 534, Issue 7605, pp. 55 - 62
Somatic mutations have been extensively characterized in breast cancer, but the effects of these genetic alterations on the proteomic landscape remain poorly... 
PATHWAYS | HETEROGENEITY | PIK3CA MUTATIONS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | GENES | BIOLOGY | RECEPTOR | EXPRESSION | SIGNATURE | REVEALS | Protein Kinases - metabolism | Focal Adhesion Kinase 1 - genetics | Receptor, Epidermal Growth Factor - genetics | Protein Kinases - genetics | Cyclin-Dependent Kinases - metabolism | Receptor, ErbB-2 - genetics | Receptors, G-Protein-Coupled - metabolism | Genomics | Humans | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Phosphoproteins - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - metabolism | Breast Neoplasms - enzymology | Receptor, Epidermal Growth Factor - metabolism | Phosphoproteins - analysis | Mass Spectrometry | src-Family Kinases - metabolism | Female | Cyclin-Dependent Kinases - genetics | Focal Adhesion Kinase 1 - metabolism | Chromosomes, Human, Pair 5 - genetics | Breast Neoplasms - classification | Chromosome Deletion | p21-Activated Kinases - genetics | Signal Transduction | Molecular Sequence Annotation | Calcium-Binding Proteins - deficiency | Phosphoproteins - genetics | Mutation - genetics | S-Phase Kinase-Associated Proteins - metabolism | p21-Activated Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Proteomics | S-Phase Kinase-Associated Proteins - genetics | Receptors, G-Protein-Coupled - genetics | src-Family Kinases - genetics | Calcium-Binding Proteins - genetics | Breast cancer | Genetic aspects | Research | Oncology, Experimental | Cancer | Physiological aspects | Methods | Mutation (Biology) | Proteins | Gene amplification | Peptides | Protein expression | Genomes | Mutation | Kinases | Deoxyribonucleic acid--DNA | Tumors | Index Medicus
Journal Article
Journal Article
Journal Article
Nature, ISSN 0028-0836, 02/2012, Volume 482, Issue 7385, pp. 419 - 422
Journal Article
Science, ISSN 0036-8075, 1/2011, Volume 331, Issue 6016, pp. 456 - 461
Adenosine monophosphate—activated protein kinase (AMPK) is a conserved sensor of intracellular energy activated in response to low nutrient availability and... 
Birds of prey | Medical research | Phosphorylation | Starvation | Mitochondria | Hepatocytes | Complementary DNA | Liver | REPORTS | Cell lines | Vehicles | TARGET | CATALYTIC SUBUNIT | METFORMIN | COMPLEX | METABOLISM | ROLES | MULTIDISCIPLINARY SCIENCES | DISEASE | C-ELEGANS | AUTOPHAGY | DOMAINS | AMP-Activated Protein Kinases - metabolism | Mitochondria, Liver - metabolism | Sequestosome-1 Protein | Humans | Caenorhabditis elegans Proteins - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Hepatocytes - metabolism | Autophagy | Autophagy-Related Protein-1 Homolog | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Cell Line | Caenorhabditis elegans - metabolism | Signal Transduction | Cell Survival | Liver - metabolism | Metformin - pharmacology | Protein-Serine-Threonine Kinases - genetics | Phenformin - pharmacology | Transcription Factors - metabolism | Insulin - metabolism | Animals | Energy Metabolism | Intracellular Signaling Peptides and Proteins - chemistry | Mitochondria, Liver - ultrastructure | Cell Line, Tumor | Mice | Protein-Serine-Threonine Kinases - chemistry | Adaptor Proteins, Signal Transducing - metabolism | Caenorhabditis elegans Proteins - genetics | Autophagy (Cytology) | Research | Properties | Protein kinases | Index Medicus | Proteins | Yeast | Adenosines | Homeostasis | Nutrients | Kinases | Survival
Journal Article
Nature Genetics, ISSN 1061-4036, 02/2015, Volume 47, Issue 3, pp. 250 - 256
Resistance to RAF-and MEK-targeted therapy is a major clinical challenge(1-4). RAF and MEK inhibitors are initially but only transiently effective in some but... 
COLON-CANCER | SURVIVAL | LUNG | ACTIVATION | INHIBITION | MELANOMA | SIGNALING PATHWAY | TRANSCRIPTION | GENETICS & HEREDITY | BRAF | KRAS | Humans | Molecular Targeted Therapy | Phosphoproteins - metabolism | Gene Knockdown Techniques | Heterografts | MAP Kinase Signaling System - genetics | HEK293 Cells | Female | MAP Kinase Kinase Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins B-raf - metabolism | MAP Kinase Kinase Kinases - genetics | Protein-Serine-Threonine Kinases - genetics | MAP Kinase Kinase Kinases - metabolism | Phosphoproteins - genetics | Mice, SCID | HT29 Cells | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Drug Resistance, Neoplasm - genetics | Animals | MAP Kinase Signaling System - drug effects | Proto-Oncogene Proteins B-raf - genetics | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Mice, Inbred NOD | Biomarkers, Tumor - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Genes, ras | Antimitotic agents | Gene mutations | Genetic aspects | Research | Antineoplastic agents | Drug resistance | Health aspects | Thyroid cancer | Lung cancer | Colorectal cancer | Melanoma | Kinases | Charitable foundations | Cancer therapies | Design of experiments | Tumors | Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 07/2010, Volume 120, Issue 7, pp. 2355 - 2369
Metformin is widely used to treat hyperglycemia in individuals with type 2 diabetes. Recently the LKB1/AMP-activated protein kinase (LKB1/AMPK) pathway was... 
MEDICINE, RESEARCH & EXPERIMENTAL | RESPIRATORY-CHAIN | SKELETAL-MUSCLE | PHOSPHOENOLPYRUVATE CARBOXYKINASE | ACTIVATED PROTEIN-KINASE | GLUCOKINASE TRANSLOCATION | GLUCOSE-METABOLISM | COACTIVATOR TORC2 | AICA RIBOSIDE | UPSTREAM KINASE | ISOLATED RAT HEPATOCYTES | Glucose-6-Phosphatase - genetics | Hypoglycemic Agents - metabolism | Diabetes Mellitus, Type 2 - genetics | Gluconeogenesis - drug effects | Diabetes Mellitus, Type 2 - metabolism | Hepatocytes - metabolism | Metformin - metabolism | AMP-Activated Protein Kinases | Hyperglycemia - genetics | Liver - drug effects | Protein-Serine-Threonine Kinases - metabolism | Liver - metabolism | Metformin - pharmacology | Mice, Inbred C57BL | Protein-Serine-Threonine Kinases - genetics | Glucose - genetics | Glucose - pharmacology | Glucose-6-Phosphatase - metabolism | Hypoglycemic Agents - pharmacology | Mice, Knockout | Hyperglycemia - metabolism | Phosphoenolpyruvate Carboxykinase (ATP) - genetics | Up-Regulation - drug effects | Animals | Gluconeogenesis - genetics | Glucose-6-Phosphatase - biosynthesis | Phosphoenolpyruvate Carboxykinase (ATP) - metabolism | Glucose - metabolism | Mice | Protein-Serine-Threonine Kinases - pharmacology | Type 2 diabetes | Control | Usage | Genetic aspects | Research | Metformin | Gene expression | Drug therapy | Health aspects | Gluconeogenesis | Index Medicus | Abridged Index Medicus | Up-Regulation | Glucose-6-Phosphatase | gluconeogenesis, animal models | Liver | Protein-Serine-Threonine Kinases | Glucose | LKB1 | Life Sciences | Hypoglycemic Agents | Phosphoenolpyruvate Carboxykinase (ATP) | Human health and pathology | Hyperglycemia | Hepatocytes | AMPK | Endocrinology and metabolism | Diabetes Mellitus, Type 2
Journal Article