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Nature (London), ISSN 1476-4687, 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 understood... 
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
Journal Article
BMC genomics, ISSN 1471-2164, 2015, Volume 16, Issue 1, p. 386
Background: The mitogen-activated protein kinase (MAPK) cascade consists of three types of reversibly phosphorylated kinases, namely, MAPK, MAPK kinase (MAPKK/MEK... 
MAPKKK | Abiotic stress | MAPKK | Biotic stress | Cucumis sativus | MAPK | Plant hormones | PROTEIN-KINASE GENE | ARABIDOPSIS-THALIANA | SATIVUS | CASCADE | PLANT-RESISTANCE | SIGNALING PATHWAY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | SEQUENCE | GENETICS & HEREDITY | BRASSICA-NAPUS L | EXPRESSION | RICE | Gene Duplication | Mitogen-Activated Protein Kinase Kinases - genetics | Genomics | Molecular Sequence Data | Cucumis sativus - genetics | Gene Expression Profiling | Cucumis sativus - physiology | Phylogeny | Promoter Regions, Genetic - genetics | Mitogen-Activated Protein Kinases - chemistry | MAP Kinase Kinase Kinases - chemistry | Mitogen-Activated Protein Kinase Kinases - metabolism | MAP Kinase Signaling System - genetics | Conserved Sequence | Transcription, Genetic | Protein-Serine-Threonine Kinases - metabolism | Multigene Family - genetics | Protein Structure, Tertiary | Amino Acid Sequence | Genome, Plant - genetics | MAP Kinase Kinase Kinases - genetics | Stress, Physiological - genetics | Protein-Serine-Threonine Kinases - genetics | Chromosome Mapping | MAP Kinase Kinase Kinases - metabolism | Cucumis sativus - growth & development | Amino Acid Motifs | Mitogen-Activated Protein Kinase Kinases - chemistry | Sequence Alignment | MAP Kinase Signaling System - drug effects | Cucumis sativus - cytology | Mitogen-Activated Protein Kinases - genetics | Protein-Serine-Threonine Kinases - chemistry | Plant Growth Regulators - pharmacology | Evolution, Molecular | Mitogen-Activated Protein Kinases - metabolism | Amino acids | Mitogens | Protein kinases
Journal Article
Cancer Cell, ISSN 1535-6108, 2010, Volume 17, Issue 6, pp. 547 - 559
In mice, Lkb1 deletion and activation of Kras G12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these... 
CELLCYCLE | SIGNALING | INACTIVATION | SUPPRESSOR | SIGNATURES | ONCOLOGY | SRC | ADENOCARCINOMA | SENSITIVITY | MUTATIONS | LKB1/STK11 | EXPRESSION | TUMORIGENESIS | CELL BIOLOGY | Lung Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - deficiency | Protein-Tyrosine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Genomics | Humans | Lung Neoplasms - metabolism | Gene Expression Profiling | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Cell Movement - genetics | Phosphorylation - genetics | RNA Interference | Gene Expression Regulation, Neoplastic - genetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - metabolism | Signal Transduction - genetics | Enzyme Inhibitors - therapeutic use | Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors | Focal Adhesion Protein-Tyrosine Kinases - genetics | Focal Adhesions - genetics | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | src-Family Kinases - genetics | Protein-Tyrosine Kinases - antagonists & inhibitors | ras Proteins - genetics | Lung Neoplasms - pathology | Cell Transdifferentiation - genetics | Protein-Tyrosine Kinases - genetics | Neoplasm Metastasis - drug therapy | Mice, Mutant Strains | Protein-Serine-Threonine Kinases - antagonists & inhibitors | src-Family Kinases - metabolism | Female | Drug Therapy, Combination | Lung Neoplasms - genetics | Cell Adhesion - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | src-Family Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Up-Regulation - genetics | Xenograft Model Antitumor Assays | Neoplasm Metastasis - genetics | Animals | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Focal Adhesions - metabolism | Proteomics | Protein Kinase Inhibitors - pharmacology | Oncology, Experimental | Analysis | Lung cancer | Development and progression | Metastasis | Research | Cancer
Journal Article
1997, Cancer surveys, ISBN 0879695188, Volume 29., vi, 363
Book
Cell death and differentiation, ISSN 1476-5403, 2014, Volume 21, Issue 10, pp. 1511 - 1521
Necroptosis is a form of programmed cell death that depends on the activation of receptor interacting protein kinase-1 (RIPK1) and RIPK3 by receptors such as... 
APOPTOSIS | RIPOPTOSOME | MLKL | MACROPHAGES | DOWNSTREAM | BIOCHEMISTRY & MOLECULAR BIOLOGY | MIXED LINEAGE KINASE | PROGRAMMED NECROSIS | DOMAIN-LIKE | CLEAVAGE | CELL-DEATH | CELL BIOLOGY | Protein Kinases - metabolism | Protein Structure, Tertiary | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Tumor Necrosis Factor-alpha - metabolism | Cell Line | Phosphorylation | Protein Kinases - genetics | Cell Survival | Humans | Protein Multimerization | Receptors, Tumor Necrosis Factor, Type I | Caspase 8 - metabolism | Imidazoles - pharmacology | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Necrosis - physiopathology | RNA Interference | Indoles - pharmacology | RNA, Small Interfering | Apoptosis - physiology | Enzyme Activation | Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Receptor-Interacting Protein Serine-Threonine Kinases/genetics | Protein Kinases/genetics | Receptor-Interacting Protein Serine-Threonine Kinases/antagonists & inhibitors | Caspase 8/metabolism | Receptor-Interacting Protein Serine-Threonine Kinases/metabolism | Tumor Necrosis Factor-alpha/antagonists & inhibitors | Indoles/pharmacology | Life Sciences | Tumor Necrosis Factor-alpha/metabolism | Imidazoles/pharmacology | Immunology | Apoptosis/physiology | Protein Kinases/metabolism | Necrosis/physiopathology | Original Paper
Journal Article
Nature genetics, ISSN 1546-1718, 2015, Volume 47, Issue 3, pp. 250 - 256
... not all patients with BRAF gene mutation and are largely ineffective in those with RAS gene mutation because of resistance(5-14). Through a genetic screen in BRAF-mutant tumor cells, we show that the Hippo pathway effector YAP... 
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 | Transcription Factors | 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
Journal Article
Nature (London), ISSN 1476-4687, 2012, Volume 482, Issue 7385, pp. 419 - 422
Journal Article
The Journal of biological chemistry, ISSN 1083-351X, 2007, Volume 282, Issue 50, pp. 36223 - 36229
The Rip2 kinase contains a caspase recruitment domain and has been implicated in the activation of the transcriptional factor NF... 
PEPTIDOGLYCAN | PROTEIN | INNATE IMMUNE-RESPONSES | HOST RECOGNITION | MACROPHAGES | BIOCHEMISTRY & MOLECULAR BIOLOGY | TOLL-LIKE RECEPTOR | SYSTEMS | NF-KAPPA-B | TLR4 | MYD88 | Mycobacterium tuberculosis - immunology | Ubiquitin - metabolism | NF-kappa B - metabolism | Nod2 Signaling Adaptor Protein - genetics | Ubiquitination - drug effects | TNF Receptor-Associated Factor 6 - genetics | Toll-Like Receptors - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - immunology | Macrophages - microbiology | MAP Kinase Kinase Kinases - genetics | Toll-Like Receptors - immunology | Myeloid Differentiation Factor 88 - genetics | Ubiquitin-Protein Ligases - metabolism | Nod2 Signaling Adaptor Protein - immunology | Ubiquitin-Conjugating Enzymes - genetics | MAP Kinase Kinase Kinases - metabolism | Ubiquitin - genetics | MAP Kinase Kinase Kinases - immunology | Mice, Knockout | Acetylmuramyl-Alanyl-Isoglutamine - pharmacology | Macrophages - metabolism | Nod2 Signaling Adaptor Protein - metabolism | Signal Transduction - drug effects | Ubiquitin-Conjugating Enzymes - metabolism | Toll-Like Receptors - genetics | I-kappa B Kinase - immunology | Mice | Ubiquitin-Protein Ligases - genetics | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Adjuvants, Immunologic - pharmacology | NF-kappa B - immunology | TNF Receptor-Associated Factor 6 - immunology | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Enzyme Activation - immunology | Signal Transduction - immunology | Ubiquitin-Protein Ligases - immunology | I-kappa B Kinase - metabolism | Myeloid Differentiation Factor 88 - immunology | Ubiquitin-Conjugating Enzymes - immunology | Tuberculosis - metabolism | Macrophages - immunology | Cells, Cultured | Ubiquitination - immunology | I-kappa B Kinase - genetics | Enzyme Activation - drug effects | Tuberculosis - immunology | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | NF-kappa B - genetics | Tuberculosis - genetics | TNF Receptor-Associated Factor 6 - metabolism | Myeloid Differentiation Factor 88 - metabolism | Ubiquitin - immunology
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2010, Volume 120, Issue 7, pp. 2355 - 2369
.... Recently the LKB1/AMP-activated protein kinase (LKB1/AMPK) pathway was proposed to mediate the action of metformin on hepatic gluconeogenesis... 
MEDICINE, RESEARCH & EXPERIMENTAL | RESPIRATORY-CHAIN | SKELETAL-MUSCLE | PHOSPHOENOLPYRUVATE CARBOXYKINASE | CYCLIC-AMP | ACTIVATED PROTEIN-KINASE | PHOSPHORYLATION | AICA RIBOSIDE | UPSTREAM KINASE | LKB1 | GLUCOSE-PRODUCTION | 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 | Up-Regulation | Glucose-6-Phosphatase | gluconeogenesis, animal models | Liver | Protein-Serine-Threonine Kinases | Glucose | Life Sciences | Hypoglycemic Agents | Phosphoenolpyruvate Carboxykinase (ATP) | Human health and pathology | Hyperglycemia | Hepatocytes | AMPK | Endocrinology and metabolism | Diabetes Mellitus, Type 2
Journal Article
by Beaumont, Robin N and Warrington, Nicole M and Cavadino, Alana and Tyrrell, Jessica and Nodzenski, Michael and Horikoshi, Momoko and Geller, Frank and Myhre, Ronny and Richmond, Rebecca C and Paternoster, Lavinia and Bradfield, Jonathan P and Kreiner-Møller, Eskil and Huikari, Ville and Metrustry, Sarah and Lunetta, Kathryn L and Painter, Jodie N and Hottenga, Jouke-Jan and Allard, Catherine and Barton, Sheila J and Espinosa, Ana and Marsh, Julie A and Potter, Catherine and Zhang, Ge and Ang, Wei and Berry, Diane J and Bouchard, Luigi and Das, Shikta and Hakonarson, Hakon and Heikkinen, Jani and Helgeland, Øyvind and Hocher, Berthold and Hofman, Albert and Inskip, Hazel M and Jones, Samuel E and Kogevinas, Manolis and Lind, Penelope A and Marullo, Letizia and Medland, Sarah E and Murray, Anna and Murray, Jeffrey C and Njølstad, Pål R and Nohr, Ellen A and Reichetzeder, Christoph and Ring, Susan M and Ruth, Katherine S and Santa-Marina, Loreto and Scholtens, Denise M and Sebert, Sylvain and Sengpiel, Verena and Tuke, Marcus A and Vaudel, Marc and Weedon, Michael N and Willemsen, Gonneke and Wood, Andrew R and Yaghootkar, Hanieh and Muglia, Louis J and Bartels, Meike and Relton, Caroline L and Pennell, Craig E and Chatzi, Leda and Estivill, Xavier and Holloway, John W and Boomsma, Dorret I and Montgomery, Grant W and Murabito, Joanne M and Spector, Tim D and Power, Christine and Järvelin, Marjo-Ritta and Bisgaard, Hans and Grant, Struan F A and Sørensen, Thorkild I A and Jaddoe, Vincent W and Jacobsson, Bo and Melbye, Mads and McCarthy, Mark I and Hattersley, Andrew T and Hayes, M Geoffrey and Frayling, Timothy M and Hivert, Marie-France and Felix, Janine F and Hyppönen, Elina and Lowe, William L and Evans, David M and Lawlor, Debbie A and Feenstra, Bjarke and Freathy, Rachel M and Early Growth Genetics (EGG) Consortium and Early Growth Genetics EGG and Institutionen för kliniska vetenskaper, Avdelningen för obstetrik och gynekologi and Sahlgrenska akademin and Göteborgs universitet and Gothenburg University and Institute of Clinical Sciences, Department of Obstetrics and Gynecology and Sahlgrenska Academy
Human molecular genetics, ISSN 1460-2083, 2018, Volume 27, Issue 4, pp. 742 - 756
Journal Article