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American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 06/2009, Volume 296, Issue 6, pp. 1258 - 1270
Myostatin is a negative regulator of skeletal muscle size, previously shown to inhibit muscle cell differentiation. Myostatin requires both Smad2 and Smad3... 
MAFbx | Mammalian target of rapamycin complex signaling | MuRF1 | S6 kinase | Smad signaling | Human skeletal muscle cells | Transducer of regulated Ca | responsive element-binding protein activity | MuRF-1 | Atrogin | Transforming growth factor-β-like molecules | IGF-I | PHYSIOLOGY | ATROPHY | RAPID DISUSE | human skeletal muscle cells | transforming growth factor-beta-like molecules | SKELETAL-MUSCLE HYPERTROPHY | FOXO TRANSCRIPTION FACTORS | UBIQUITIN LIGASES | transducer of regulated Ca2+-responsive element-binding protein activity | CELL BIOLOGY | atrogin | PATHWAY | GROWTH | GENE-EXPRESSION | mammalian target of rapamycin complex signaling | CONDITIONAL ACTIVATION | Activin Receptors, Type I - antagonists & inhibitors | Protein Kinases - metabolism | Phosphorylation | Protein Kinases - genetics | Humans | Smad3 Protein - metabolism | Muscle Fibers, Skeletal - drug effects | Tripartite Motif Proteins | Smad3 Protein - genetics | Transfection | RNA Interference | Myoblasts, Skeletal - pathology | Smad2 Protein - genetics | Muscle Proteins - metabolism | Dioxoles - pharmacology | Regulatory-Associated Protein of mTOR | Benzamides - pharmacology | Myostatin - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Rapamycin-Insensitive Companion of mTOR Protein | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Signal Transduction | Cell Size - drug effects | Cells, Cultured | Smad2 Protein - metabolism | Ubiquitin-Protein Ligases - metabolism | Organ Size | Activin Receptors, Type I - metabolism | Myoblasts, Skeletal - enzymology | SKP Cullin F-Box Protein Ligases - metabolism | Mice, SCID | Myostatin - antagonists & inhibitors | Adaptor Proteins, Signal Transducing | Animals | Carrier Proteins - metabolism | Proteins - metabolism | Cell Differentiation - drug effects | Follistatin - pharmacology | Muscle Fibers, Skeletal - pathology | Creatine Kinase - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | TOR Serine-Threonine Kinases | Myoblasts, Skeletal - drug effects | Insulin-Like Growth Factor I - metabolism | Muscle Fibers, Skeletal - enzymology | RNA, Small Interfering - metabolism
Journal Article
Nature, ISSN 0028-0836, 05/2016, Volume 533, Issue 7604, pp. 493 - 498
Journal Article
PLoS ONE, ISSN 1932-6203, 01/2013, Volume 8, Issue 1, p. e54001
Background: Histone deacetylase (HDAC) inhibitors are promising anti-fibrosis drugs; however, nonselective inhibition of class I and class II HDACs does not... 
GROWTH-FACTOR-BETA | SOLID TUMORS | OBSTRUCTIVE NEPHROPATHY | MULTIDISCIPLINARY SCIENCES | CARDIAC-HYPERTROPHY | INTERSTITIAL FIBROSIS | INJURY | ANGIOTENSIN-II | CHRONIC KIDNEY-DISEASE | FACTOR RECEPTOR | MOLECULAR-MECHANISMS | Kidney - pathology | Transforming Growth Factor beta1 - metabolism | Actins - metabolism | Smad3 Protein - metabolism | Ureteral Obstruction - metabolism | Leukocytes - immunology | Kidney - metabolism | Receptor, Epidermal Growth Factor - metabolism | Benzamides - therapeutic use | Benzamides - pharmacology | Phosphorylation - drug effects | Ureteral Obstruction - drug therapy | Protein-Serine-Threonine Kinases - metabolism | Transforming Growth Factor beta1 - biosynthesis | Fibroblasts - metabolism | Pyridines - therapeutic use | Collagen Type I - metabolism | Kidney - drug effects | Histone Deacetylases - metabolism | Fibroblasts - pathology | Fibronectins - metabolism | Ureteral Obstruction - immunology | Gene Expression Regulation - drug effects | Acetylation - drug effects | Animals | Receptors, Transforming Growth Factor beta - metabolism | Signal Transduction - drug effects | Cell Cycle Checkpoints - drug effects | Fibroblasts - drug effects | Ureteral Obstruction - pathology | Fibrosis | Histone Deacetylase Inhibitors - pharmacology | Leukocytes - drug effects | Cell Proliferation - drug effects | Histone Deacetylase Inhibitors - therapeutic use | Mice | Pyridines - pharmacology | Histones - metabolism | Fibronectins | Muscle proteins | Growth factors | Collagen | Analysis | Drugs | Histone deacetylase | Phosphorylation | Smad protein | Animal models | Collagen (type I) | Nephrology | Transcription | Syngeneic grafts | Transforming growth factor-b | Smooth muscle | Activation | Kinases | Fibronectin | Medical schools | Epidermal growth factor | Actin | Rodents | Cell cycle | Fibroblasts | Ureter | Inhibition | Kidneys | Transforming growth factor-b1 | Epidermal growth factor receptors | Pulmonary arteries | Fibrils | Muscles | Medicine | Signaling | Hospitals | Kidney diseases | Cancer
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 08/2016, Volume 23, Issue 8, pp. 1271 - 1282
In order for cancer cells to survive during metastasis, they must overcome anoikis, a caspase-dependent cell death process triggered by extracellular matrix... 
COLON-CANCER | SURVIVAL | BREAST-CANCER CELLS | APOPTOSIS | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | PROSTATE-CANCER | TUMOR-SUPPRESSOR | AKT | SERUM | PHLPP | CELL BIOLOGY | Caspase 7 - metabolism | ras Proteins - genetics | Humans | Phosphoprotein Phosphatases - metabolism | Caspase 3 - metabolism | Extracellular Matrix - metabolism | ras Proteins - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Immediate-Early Proteins - metabolism | RNA Interference | Adenosine Triphosphate - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Benzamides - pharmacology | p38 Mitogen-Activated Protein Kinases - metabolism | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Protein-Serine-Threonine Kinases - metabolism | Hydrazines - pharmacology | HCT116 Cells | Protein-Serine-Threonine Kinases - genetics | ras Proteins - antagonists & inhibitors | Nuclear Proteins - metabolism | Phosphoprotein Phosphatases - antagonists & inhibitors | Down-Regulation - drug effects | Immediate-Early Proteins - genetics | Phosphoprotein Phosphatases - genetics | Signal Transduction - drug effects | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Glucose - metabolism | Anoikis - drug effects | Immediate-Early Proteins - antagonists & inhibitors | RNA, Small Interfering - metabolism | Original Paper
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2014, Volume 9, Issue 2, p. e87915
Neuroimmune gene induction is involved in many brain pathologies including addiction. Although increased expression of proinflammatory cytokines has been found... 
INDUCED NEUROINFLAMMATION | SLICE CULTURES | CELLS | CHROMATIN PROTEIN HMGB1 | MULTIDISCIPLINARY SCIENCES | MOBILITY GROUP BOX-1 | SPINAL-CORD | INDUCTION | ALCOHOL-DRINKING | NF-KAPPA-B | RECEPTOR 4 | Microglia - metabolism | Entorhinal Cortex - metabolism | Humans | Cytosol - drug effects | Hippocampus - drug effects | Brain - metabolism | Naltrexone - pharmacology | Cell Nucleus - metabolism | HMGB1 Protein - metabolism | Inflammation Mediators - metabolism | Benzamides - pharmacology | Neurons - metabolism | Toll-Like Receptor 4 - antagonists & inhibitors | Neurons - drug effects | Hydroxamic Acids - pharmacology | Cytokines - metabolism | Microglia - drug effects | Rats | Histone Deacetylases - metabolism | Entorhinal Cortex - drug effects | Toll-Like Receptor 4 - metabolism | Blotting, Western | Brain - drug effects | Gene Expression Regulation - drug effects | Hippocampus - metabolism | Acetylation - drug effects | Ethanol - pharmacology | Animals | Signal Transduction - drug effects | Models, Biological | Cytosol - metabolism | Histone Deacetylase Inhibitors - pharmacology | Mice | Pyridines - pharmacology | Cell Nucleus - drug effects | Brain - immunology | Brain research | Alcohol, Denatured | Chromosomal proteins | Cytokines | RNA | Neurons | Analysis | Alcohol | Brain | Drug abuse | Histone deacetylase | Neurosciences | Spinal cord | Brain slice preparation | Neurobiology | Biology | Activation | Kinases | Experiments | HMGB1 protein | Proteins | Neurodegeneration | Toll-like receptors | Immune system | Translocation | Glycyrrhizin | Ethanol | Alcoholism | Cultures | Hazards | Inflammation | TLR4 protein | Tumor necrosis factor-α | IL-1β | Gene expression | Addictions | Studies | Cortex (entorhinal) | Signaling | Hypotheses | Inhibitors | Addiction | Ligands | Laboratory animals | Hippocampus | Apoptosis
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 10/2010, Volume 207, Issue 11, pp. 2331 - 2341
Foxp3-expressing regulatory T (T reg) cells have been implicated in parasite-driven inhibition of host immunity during chronic infection. We addressed whether... 
B-CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | TH2 RESPONSES | PROTECTIVE IMMUNITY | TRANSCRIPTION FACTOR FOXP3 | IN-VIVO | AIRWAY INFLAMMATION | NEMATODE INFECTION | POLYGYRUS INFECTION | IMMUNOLOGY | ORAL ANTIGEN | AUTOIMMUNE-DISEASE | Receptors, Transforming Growth Factor beta - genetics | Strongylida Infections - metabolism | Receptors, Transforming Growth Factor beta - immunology | Smad3 Protein - immunology | Nematospiroides dubius - metabolism | Th2 Cells - immunology | T-Lymphocytes, Regulatory - immunology | Th1 Cells - metabolism | Host-Parasite Interactions - genetics | Phosphorylation - genetics | Smad2 Protein - genetics | Dioxoles - pharmacology | Phosphorylation - immunology | Protein-Serine-Threonine Kinases - metabolism | Smad2 Protein - metabolism | Mice, Transgenic | Signal Transduction - genetics | Antigens, Helminth - immunology | Receptors, Transforming Growth Factor beta - antagonists & inhibitors | Signal Transduction - drug effects | Mice | Mice, Inbred BALB C | Chronic Disease | Forkhead Transcription Factors - immunology | T-Lymphocytes, Regulatory - metabolism | Antigens, Helminth - metabolism | Strongylida Infections - genetics | Smad3 Protein - metabolism | Th1 Cells - immunology | Nematospiroides dubius - immunology | Signal Transduction - immunology | Smad3 Protein - genetics | Strongylida Infections - immunology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Benzamides - pharmacology | Transforming Growth Factor beta - immunology | Forkhead Transcription Factors - biosynthesis | Gene Expression Regulation - genetics | Gene Expression Regulation - immunology | Protein-Serine-Threonine Kinases - genetics | Host-Parasite Interactions - immunology | Forkhead Transcription Factors - genetics | Th2 Cells - metabolism | Gene Expression Regulation - drug effects | Host-Parasite Interactions - drug effects | Smad2 Protein - immunology | Animals | Transforming Growth Factor beta - genetics | Receptors, Transforming Growth Factor beta - metabolism | Protein-Serine-Threonine Kinases - immunology | Cell Proliferation - drug effects | Transforming Growth Factor beta - metabolism
Journal Article
Science, ISSN 0036-8075, 8/2009, Volume 325, Issue 5942, pp. 834 - 840
Journal Article
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 431 - 435
Activating mutations in KRAS and BRAF are found in more than 30% of all human tumours and 40% of melanoma, respectively, thus targeting this pathway could have... 
SELECTIVE INHIBITOR | POTENT | EFFICACY | MECHANISM | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | KINASE | C-RAF | B-RAF | MUTATIONS | PROTEINS | Neoplasms - metabolism | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Diphenylamine - pharmacology | raf Kinases - antagonists & inhibitors | Humans | Protein Multimerization | ras Proteins - metabolism | Protein Transport - drug effects | Extracellular Signal-Regulated MAP Kinases - metabolism | raf Kinases - metabolism | Diphenylamine - analogs & derivatives | Mitogen-Activated Protein Kinase Kinases - metabolism | Adenosine Triphosphate - metabolism | Indoles - pharmacology | Benzamides - pharmacology | Cell Membrane - metabolism | raf Kinases - genetics | Cell Membrane - drug effects | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Pyrazoles - pharmacology | Protein Structure, Tertiary | Proto-Oncogene Proteins - metabolism | Cell Line | Indenes - pharmacology | raf Kinases - chemistry | Proto-Oncogene Proteins c-raf - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Neoplasms - enzymology | Proto-Oncogene Proteins - genetics | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Proto-Oncogene Proteins c-raf - metabolism | Neoplasms - drug therapy | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Proto-Oncogene Proteins c-raf - deficiency | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Neoplasms - pathology | Ras genes | Growth | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Mitogen-activated protein kinases | Competition | Clinical trials | Enzymes | Kinases | Proteins | Cellular | Inhibitors | Pathways | Tumours | Signalling | Dimerization
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 06/2006, Volume 116, Issue 6, pp. 1561 - 1570
Metastasis is the major cause of cancer morbidity, but strategies for direct interference with invasion processes are lacking. Dedifferentiated, late-stage... 
BREAST-CANCER | MEDICINE, RESEARCH & EXPERIMENTAL | FACTOR-BETA | 3D CULTURES | GROWTH-FACTOR-RECEPTOR | TRANSFORMED PHENOTYPE | EPITHELIAL-MESENCHYMAL TRANSITIONS | CELL-LINES | NF-KAPPA-B | MOLECULAR-MECHANISMS | INCREASED MALIGNANCY | Humans | ras Proteins - metabolism | Mammary Tumor Virus, Mouse - metabolism | Piperazines - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Mammary Neoplasms, Experimental - metabolism | Recombinant Fusion Proteins - metabolism | Pyrimidines - metabolism | Breast Neoplasms - metabolism | Antineoplastic Agents - metabolism | Epithelial Cells - physiology | Neoplasm Metastasis | Mammary Neoplasms, Experimental - pathology | Female | Epithelial Cells - cytology | Cell Differentiation - physiology | Receptor, Platelet-Derived Growth Factor beta - metabolism | Autocrine Communication | Receptor, Platelet-Derived Growth Factor alpha - metabolism | Mice, Transgenic | Imatinib Mesylate | Animals | Transforming Growth Factor beta - genetics | Breast Neoplasms - pathology | Mice, Nude | Cell Line, Tumor | Mesoderm - physiology | Recombinant Fusion Proteins - genetics | Signal Transduction - physiology | Mice | Benzamides | Enzyme Activation | Mammary Tumor Virus, Mouse - genetics | Transforming Growth Factor beta - metabolism | Apoptosis | Protein Kinase Inhibitors - metabolism | Medicine, Experimental | Medical research | Breast cancer | Research | Metastasis | Drug therapy
Journal Article