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Cancer Cell, ISSN 1535-6108, 2010, Volume 17, Issue 6, pp. 547 - 559
In mice, deletion and activation of results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and... 
CELLCYCLE | SIGNALING | EPITHELIAL-MESENCHYMAL TRANSITION | ONCOGENIC K-RAS | CANCER-CELLS | SUPPRESSOR | GENE | ONCOLOGY | SRC | KINASE INHIBITOR | EXPRESSION PROFILES | MUTATIONS | TUMORIGENESIS | 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 | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 9/1998, Volume 95, Issue 19, pp. 11211 - 11216
Journal Article
Molecular Cell, ISSN 1097-2765, 01/2014, Volume 53, Issue 2, pp. 193 - 208
Journal Article
Journal Article
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
Hypertension, ISSN 0194-911X, 02/2011, Volume 57, Issue 2, pp. 245 - 254
Vascular oxidative stress and inflammation play an important role in angiotensin II–induced hypertension, and mitogen-activated protein kinases participate in... 
vascular inflammation | arterial | MK2 | hypertension | angiotensin II | oxidative stress | NADPH OXIDASE | ENDOTHELIAL DYSFUNCTION | ORGAN DAMAGE | SUPEROXIDE ANION PRODUCTION | BLOOD-PRESSURE | P38 MAP KINASE | NAD(P)H OXIDASE | DIFFERENTIAL ACTIVATION | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | Inflammation - chemically induced | Cell Proliferation | Muscle, Smooth, Vascular - metabolism | Oxidative Stress | Blood Pressure - genetics | NADPH Oxidases - metabolism | Male | NF-kappa B - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Aorta - metabolism | Inflammation - metabolism | RNA Interference | Hypertension - chemically induced | Superoxides - metabolism | Blood Pressure - physiology | Chemokine CCL2 - metabolism | Aorta - physiopathology | Angiotensin II | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Mice, Inbred C57BL | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Chemokine CCL2 - genetics | Muscle, Smooth, Vascular - cytology | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Hypertension - physiopathology | Hypertension - metabolism | Mice, Knockout | Animals | Mice | Vascular Cell Adhesion Molecule-1 - metabolism | Inflammation - physiopathology | Index Medicus
Journal Article
International Journal of Oncology, ISSN 1019-6439, 12/2014, Volume 45, Issue 6, pp. 2267 - 2277
Leiomyosarcomas remain challenging tumors to manage and novel therapy strategies besides radiation and conventional chemotherapy are needed. Targeting... 
leiomyosarcoma | VEGF | tumor | angiogenesis | receptor tyrosine kinase | VEGF receptor | PTK787/ZK222584 | small molecule inhibitor | Angiogenesis | Leiomyosarcoma | Receptor tyrosine kinase | Tumor | Small molecule inhibitor | FACTOR VEGF | MIGRATION | PHASE-III | METASTATIC COLORECTAL ADENOCARCINOMA | CANCER | ANTIANGIOGENIC THERAPY | HEPATOCELLULAR-CARCINOMA | ONCOLOGY | ENDOTHELIAL GROWTH-FACTOR | Human Umbilical Vein Endothelial Cells | Vascular Endothelial Growth Factor A - biosynthesis | Vascular Endothelial Growth Factor Receptor-1 - antagonists & inhibitors | Vascular Endothelial Growth Factor Receptor-3 - biosynthesis | Humans | Proto-Oncogene Proteins c-sis - administration & dosage | Vascular Endothelial Growth Factor A - antagonists & inhibitors | Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors | Angiogenesis Inhibitors - administration & dosage | Leiomyosarcoma - genetics | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Vascular Endothelial Growth Factor Receptor-2 - biosynthesis | Gene Expression Regulation, Neoplastic - drug effects | Vascular Endothelial Growth Factor A - administration & dosage | Proto-Oncogene Proteins c-sis - biosynthesis | Phthalazines - administration & dosage | Pyridines - administration & dosage | Leiomyosarcoma - pathology | Vascular Endothelial Growth Factor Receptor-1 - biosynthesis | Cell Movement - drug effects | Protein Kinase Inhibitors - administration & dosage | Receptor Protein-Tyrosine Kinases - genetics | Signal Transduction - drug effects | Neovascularization, Pathologic - drug therapy | Cell Line, Tumor | Leiomyosarcoma - drug therapy | Neovascularization, Pathologic - genetics | Vascular Endothelial Growth Factor Receptor-3 - antagonists & inhibitors | Physiological aspects | Research | Angiogenesis inhibitors | Drug therapy | Vascular endothelial growth factor | Health aspects | Biotechnology | Laboratories | Cloning | Clinical trials | Metastasis | Kinases | Cancer therapies | Cell adhesion & migration | Studies | Cell growth | Chemotherapy | Medical prognosis | Ligands | Growth factors | Veins & arteries | Apoptosis
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 04/2013, Volume 288, Issue 16, pp. 11216 - 11232
Understanding the regulation of cardiomyocyte growth is crucial for the management of adverse ventricular remodeling and heart failure. MicroRNA-378 (miR-378)... 
MUTATIONS CAUSE NOONAN | SIGNALING PATHWAYS | PRESSURE-OVERLOAD | CARDIOMYOCYTE | BIOCHEMISTRY & MOLECULAR BIOLOGY | THERAPEUTIC TARGET | HEART-FAILURE | GENE-EXPRESSION | DIACYLGLYCEROL-BINDING MOTIFS | NUCLEOTIDE-RELEASING PROTEIN | FOCAL ADHESION KINASE | ras Proteins - genetics | ras Proteins - metabolism | Cardiomegaly - pathology | Glycogen Synthase Kinase 3 beta | MicroRNAs - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Adrenergic alpha-1 Receptor Agonists - adverse effects | Adrenergic alpha-1 Receptor Agonists - pharmacology | MAP Kinase Signaling System | MAP Kinase Kinase 1 - genetics | Phenylephrine - adverse effects | Phenylephrine - pharmacology | GRB2 Adaptor Protein - genetics | Muscle Proteins - metabolism | Proto-Oncogene Proteins c-raf | Mitogen-Activated Protein Kinase 3 - genetics | Gene Expression Regulation - genetics | MAP Kinase Kinase Kinases - genetics | Cells, Cultured | Rats | MAP Kinase Kinase 1 - metabolism | MAP Kinase Kinase Kinases - metabolism | Glycogen Synthase Kinase 3 - metabolism | Rats, Sprague-Dawley | Gene Expression Regulation - drug effects | Muscle Proteins - genetics | Phosphatidylinositol 3-Kinases - genetics | Proto-Oncogene Proteins c-akt | Animals | Glycogen Synthase Kinase 3 - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | GRB2 Adaptor Protein - biosynthesis | Cardiomegaly - chemically induced | MicroRNAs - genetics | Cardiomegaly - genetics | Cardiomegaly - metabolism | Index Medicus | Molecular Bases of Disease | MAP Kinases (MAPKs) | Molecular Biology | RNA | Ras | Cell Signaling | MicroRNA-378 | Grb2 | Cardiac Hypertrophy
Journal Article
Journal of Nutrition, ISSN 0022-3166, 2016, Volume 146, Issue 3, pp. 501 - 508
Background: The tight junctions (TJs) are essential for maintenance of the intestinal mucosal barrier integrity. Results of our recent work show that dietary... 
AMPK | Tight junction | CaMKK2 | L-glutamine | Intestinal epithelial cells | intestinal epithelial cells | PERMEABILITY | MEMBRANE | BARRIER FUNCTION | COMPONENTS | CALCIUM REGULATION | SUPPLEMENTATION | NUTRITION & DIETETICS | AMINO-ACIDS | HEALTH | EXPRESSION | tight junction | CACO-2 CELLS | Intestines - drug effects | AMP-Activated Protein Kinases - metabolism | Intestinal Mucosa - metabolism | Phosphorylation | Epithelial Cells - metabolism | Claudin-4 - genetics | Enterocytes - metabolism | Epithelial Cells - drug effects | Zonula Occludens-2 Protein - metabolism | Intestinal Mucosa - drug effects | Occludin - metabolism | Occludin - genetics | Swine | Claudin-4 - metabolism | Cell Membrane - metabolism | Glutamine - pharmacology | Zonula Occludens-1 Protein - metabolism | Cell Membrane - drug effects | Tight Junctions - drug effects | Animals, Newborn | Tight Junctions - metabolism | Zonula Occludens-1 Protein - genetics | Signal Transduction | Enterocytes - cytology | Gene Expression Regulation | Calcium-Calmodulin-Dependent Protein Kinase Kinase - genetics | Zonula Occludens-2 Protein - genetics | Animals | Enterocytes - drug effects | Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism | Junctional Adhesion Molecules - genetics | Cell Proliferation - drug effects | AMP-Activated Protein Kinases - genetics | Junctional Adhesion Molecules - metabolism | Intestines - cytology | Physiological aspects | Dosage and administration | Food and nutrition | Protein kinases | Intestinal mucosa | Methods | Glutamine | Permeability | Dietary supplements | Membrane proteins | Index Medicus
Journal Article