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American Journal of Physiology: Cell Physiology, ISSN 1522-1563, 2009, Volume 296, Issue 6, pp. C1258 - C1270
... , growth differentiation factor 11 (GDF-11), activins, bone morphogenetic protein 2 (BMP-2) and BMP-7. Myostatin inhibits activation of the Akt/mammalian target of rapamycin... 
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
Scientific reports, ISSN 2045-2322, 2018, Volume 8, Issue 1, pp. 998 - 10
.... And histological evaluation and protein expressions of irradiated tissue were analyzed to confirm the potential anti-fibrosis effect of JQ1 and its underlying mechanisms... 
CANCER PATIENTS | BROMODOMAINS | TGF-BETA | THERAPY | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | BRD4 INHIBITION | PNEUMONITIS | MECHANISMS | PULMONARY-FIBROSIS | NORMAL TISSUE-INJURY | Humans | NF-kappa B - metabolism | Smad2 Protein - antagonists & inhibitors | Collagen Type I - genetics | MCF-7 Cells | Smad2 Protein - genetics | Lung - radiation effects | Pulmonary Fibrosis - etiology | Fibroblasts - metabolism | NF-kappa B - antagonists & inhibitors | Smad2 Protein - metabolism | Rats | Pulmonary Fibrosis - pathology | Rats, Sprague-Dawley | Smad3 Protein - antagonists & inhibitors | Fibroblasts - drug effects | Proto-Oncogene Proteins c-myc - antagonists & inhibitors | Pulmonary Fibrosis - prevention & control | Cell Line, Tumor | Gene Expression Regulation - radiation effects | Fibroblasts - cytology | Proto-Oncogene Proteins c-myc - genetics | Hydroxyproline - antagonists & inhibitors | Proteins - antagonists & inhibitors | Gamma Rays - adverse effects | Hydroxyproline - biosynthesis | Pulmonary Fibrosis - genetics | Smad3 Protein - metabolism | Molecular Targeted Therapy | Smad3 Protein - genetics | Transforming Growth Factor beta - antagonists & inhibitors | Female | Lung - metabolism | Nuclear Proteins - genetics | Lung - pathology | Collagen Type I - metabolism | Collagen Type I - antagonists & inhibitors | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Transcription Factors - genetics | Proto-Oncogene Proteins c-myc - metabolism | Azepines - pharmacology | Gene Expression Regulation - drug effects | Proteins - genetics | Transcription Factors - metabolism | Triazoles - pharmacology | Animals | Proteins - metabolism | Transforming Growth Factor beta - genetics | Fibroblasts - radiation effects | NF-kappa B - genetics | Nuclear Proteins - antagonists & inhibitors | Cell Proliferation - drug effects | Transforming Growth Factor beta - metabolism | NF-κB protein | Collagen (type I) | Animal models | Cell survival | Lung diseases | Hydroxyproline | Radiation | c-Myc protein | Smad3 protein | Thorax | Breast cancer | Inflammation | Radiation therapy | Myc protein | Esophagus | Computed tomography | Smad2 protein | Rodents | Fibrosis | Fibroblasts | Cancer
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2012, Volume 7, Issue 5, p. e36964
Articular cartilage is physiologically exposed to repeated loads. The mechanical properties of cartilage are due to its extracellular matrix, and homeostasis... 
ADHESION | SHEAR | TGF-BETA | PROTEIN | BOVINE ARTICULAR CHONDROCYTES | MULTIDISCIPLINARY SCIENCES | ENDOTHELIAL-CELLS | KINASE | MECHANICAL STIMULATION | FLOW | PRIMARY CILIA | Chondrocytes - cytology | Phosphorylation | Transcription Factor AP-1 - genetics | Stress, Mechanical | Transcription Factor AP-1 - metabolism | Cartilage, Articular - physiology | MAP Kinase Signaling System - genetics | Chondrocytes - physiology | Cartilage, Articular - metabolism | Early Growth Response Protein 1 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Mechanotransduction, Cellular - genetics | Chondrocytes - metabolism | Extracellular Matrix Proteins - metabolism | Hydrogel, Polyethylene Glycol Dimethacrylate - metabolism | Signal Transduction | Cartilage, Articular - cytology | Down-Regulation | Extracellular Matrix Proteins - genetics | p38 Mitogen-Activated Protein Kinases - genetics | Smad Proteins - genetics | Sepharose - metabolism | Animals | Transforming Growth Factor beta - genetics | Mitogen-Activated Protein Kinases - genetics | Mice | Smad Proteins - metabolism | Transforming Growth Factor beta - metabolism | Early Growth Response Protein 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | DNA microarrays | Analysis | Genes | Physiological aspects | Mechanical properties | Bone morphogenetic proteins | Transforming growth factors | Gene expression | Mitogens | Protein kinases | Compression | Transcription factors | Hydrogels | Genomics | Transforming growth factor-a | Homeostasis | Genomes | Shear stresses | Kinases | Western blotting | Proteins | Cartilage | Signal transduction | Pathways | Smad2 protein | Atherosclerosis | Extracellular matrix | Data analysis | Extracellular signal-regulated kinase | MAP kinase | Cartilage (articular) | Metabolism | Signaling | Embedded systems | Protein kinase | Collagen | Chondrocytes | Mitogen-Activated Protein Kinases | Sepharose | Biochemistry, Molecular Biology | Cartilage, Articular/physiology | Cartilage, Articular/cytology | Transcription Factor AP-1 | MAP Kinase Signaling System | Life Sciences | Mechanotransduction, Cellular | Hydrogel, Polyethylene Glycol Dimethacrylate | Extracellular Matrix Proteins | Smad Proteins | Early Growth Response Protein 1 | p38 Mitogen-Activated Protein Kinases | Transforming Growth Factor beta | Cartilage, Articular/metabolism
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 12/2010, Volume 17, Issue 12, pp. 1867 - 1881
.... As2O3 reduced the protein expression of EVI1, TAK1, SMAD2/3, and TGF beta RII while increasing SnoN/SkiL... 
ecotropic viral integration site-1 (EVI1) | arsenic trioxide (As | autophagy | transforming growth factor-β (TGFβ) | SnoN/SkiL | ovarian cancer | APOPTOSIS | ONCOPROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | arsenic trioxide (As2O3) | DEATH | PROLIFERATION | CANCER | CELL BIOLOGY | GROWTH-FACTOR-BETA | ONCOGENE | INHIBITION | transforming growth factor-beta (TGF beta) | GLUTATHIONE | LEUKEMIA | ovarian cancer, ecotropic viral integration site-1 (EVI1) | Reactive Oxygen Species - metabolism | Microtubule-Associated Proteins - genetics | Arsenicals | Microtubule-Associated Proteins - metabolism | Humans | Intracellular Signaling Peptides and Proteins - metabolism | Autophagy | RNA Interference | Apoptosis Regulatory Proteins - genetics | Female | Membrane Proteins - metabolism | Ovarian Neoplasms - metabolism | Intracellular Signaling Peptides and Proteins - genetics | Beclin-1 | Proto-Oncogene Proteins - metabolism | Ubiquitin-Activating Enzymes - genetics | Arsenic Trioxide | Signal Transduction | Membrane Proteins - genetics | Oxides - toxicity | Proto-Oncogene Proteins - genetics | Ubiquitin-Activating Enzymes - metabolism | Apoptosis Regulatory Proteins - metabolism | Autophagy-Related Protein 7 | Poly(ADP-ribose) Polymerases - metabolism | Autophagy-Related Protein 5 | Acetylcysteine - pharmacology | Cell Line, Tumor | Carcinoma - metabolism | Multidrug Resistance-Associated Proteins - metabolism | Transforming Growth Factor beta - metabolism | RNA, Small Interfering - metabolism | Ubiquitin | Cell survival | Evi1 protein | Ovarian carcinoma | TAK1 protein | Multidrug resistance | Phagosomes | Arsenic trioxide | siRNA | Transforming growth factor- beta | Promyeloid leukemia | Signal transduction | Vesicles | Transmission electron microscopy | Smad2 protein | N-Acetyl-L-cysteine | Immunofluorescence | Phagocytosis | Apoptosis | apoptosis | reactive oxygen species (ROS) | SkiL | SnoN | multidrug resistance protein (MRP1)
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2013, Volume 8, Issue 10, p. e77300
...) stress fibers was used to visualize myofibroblasts. Protein and phosphoprotein were determined by Western blotting... 
CELLS | ACTIVATION | POSITIVE FEEDBACK | MAP KINASE | MULTIDISCIPLINARY SCIENCES | TISSUE FIBROSIS | RECEPTOR | OXIDASE EXPRESSION | DIFFERENTIATION | FIBROBLASTS | KERATOCYTES | Corneal Opacity - chemically induced | Reactive Oxygen Species - metabolism | Calcium - metabolism | Humans | Actins - metabolism | Corneal Opacity - metabolism | Mitogen-Activated Protein Kinase 9 - genetics | Actins - genetics | Myofibroblasts - metabolism | TRPV Cation Channels - metabolism | Swine | TRPV Cation Channels - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - genetics | Smad2 Protein - genetics | Mitogen-Activated Protein Kinase 8 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Corneal Injuries | Alkalies | Myofibroblasts - pathology | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Mitogen-Activated Protein Kinase 9 - metabolism | Tissue Culture Techniques | Mitogen-Activated Protein Kinase 8 - metabolism | Gene Expression Regulation | Smad2 Protein - metabolism | p38 Mitogen-Activated Protein Kinases - genetics | Corneal Opacity - genetics | TRPV Cation Channels - genetics | Cornea - metabolism | Transforming Growth Factor beta - pharmacology | Feedback, Physiological | Animals | Transforming Growth Factor beta - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Mice | Transforming Growth Factor beta - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Cell culture | Flow cytometry | Oxidative stress | Phosphorylation | Cornea | Reactive oxygen species | Transparency | Smooth muscle | Capsaicin receptors | Activation | Feedback loops | Positive feedback | Calcium influx | Western blotting | Proteins | Transient receptor potential proteins | Transfection | Restoration | Protein folding | Actin | Smad2 protein | Fibroblasts | Growth factors | Phenotypes | Oxygen | Wound healing | Calcium (intracellular) | Muscles | Extracellular signal-regulated kinase | Optometry | siRNA | Gene expression | Capsazepine | Medicine | Cytometry | Gene flow | Calcium ions
Journal Article
Nature communications, ISSN 2041-1723, 2019, Volume 10, Issue 1, pp. 3616 - 19
...: human and murine dilated cardiomyopathy and repaired tetralogy of Fallot. Transgenic mice lacking the N-terminal region of the WWP2 protein show improved cardiac... 
TGF-BETA | RAT | FIBROBLAST | MULTIDISCIPLINARY SCIENCES | HEART-FAILURE | GENE-EXPRESSION | DETERMINANT | IDENTIFICATION | BLOOD-PRESSURE | E3 UBIQUITIN LIGASE | REVEALS | Heart Diseases - metabolism | Humans | Middle Aged | Male | Fibrosis - metabolism | Gene Regulatory Networks | Young Adult | Cardiomyopathies - genetics | Smad2 Protein - genetics | Adult | Female | Extracellular Matrix Proteins - metabolism | Fibrosis - genetics | Genetic Predisposition to Disease - genetics | Gene Expression Regulation | Smad2 Protein - metabolism | Ubiquitin-Protein Ligases - metabolism | Mice, Transgenic | Animals | Cardiomyopathies - metabolism | Protein Isoforms | Adolescent | Aged | Mice | Ubiquitin-Protein Ligases - genetics | Transforming Growth Factor beta - metabolism | Heart Diseases - genetics | Myocardial infarction | Ubiquitin | Translocation | Tetralogy of Fallot | Transcription | Cardiomyopathy | Transgenic mice | Gene expression | Coronary artery disease | Nuclear transport | Dilated cardiomyopathy | Smad2 protein | Fibrosis | Isoforms | Fibroblasts | Genetics | Extracellular matrix | Cardiovascular diseases | Heart diseases | Ubiquitin-protein ligase | Populations and Evolution | Ubiquitin-Protein Ligases / metabolism | Smad2 Protein / metabolism | Smad2 Protein / genetics | Genetic Predisposition to Disease / genetics | Fibrosis / genetics | Cardiomyopathies / metabolism | Life Sciences | Transforming Growth Factor beta / metabolism | Extracellular Matrix Proteins / metabolism | Fibrosis / metabolism | Cardiomyopathies / genetics | Heart Diseases / genetics | Ubiquitin-Protein Ligases / genetics | Heart Diseases / metabolism | Human genetics
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 06/2016, Volume 291, Issue 23, pp. 12184 - 12194
.... However, mechanisms underlying atrophy remain unclear. Here, we show that skeletal muscle immobilization elevates Smad2/3 protein but not mRNA levels in muscle, promoting atrophy... 
HYPERTROPHY | MYOSTATIN GENE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CAPILLARY-ELECTROPHORESIS | RECEPTOR | MICE | FOXO TRANSCRIPTION FACTORS | F-BOX PROTEIN | MASS-SPECTROMETRY | GROWTH-FACTOR-I | SCF UBIQUITIN LIGASE | Receptor, IGF Type 1 - metabolism | Insulin-Like Growth Factor I - pharmacology | SKP Cullin F-Box Protein Ligases - genetics | Amino Acids, Branched-Chain - metabolism | Muscle Denervation | Muscle, Skeletal - innervation | Muscle, Skeletal - metabolism | Smad3 Protein - metabolism | Muscle Fibers, Skeletal - drug effects | Muscle Fibers, Skeletal - metabolism | Smad3 Protein - genetics | Smad2 Protein - genetics | Muscle Proteins - metabolism | Myostatin - genetics | Restraint, Physical - adverse effects | Myostatin - metabolism | Muscular Atrophy - etiology | Cell Line | Muscular Atrophy - metabolism | Smad2 Protein - metabolism | Ubiquitin-Protein Ligases - metabolism | Tripartite Motif Proteins - genetics | Mice, Transgenic | SKP Cullin F-Box Protein Ligases - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Receptor, IGF Type 1 - genetics | Blotting, Western | Mice, Knockout | Muscle Proteins - genetics | Animals | Glucose - metabolism | Muscle Fibers, Skeletal - cytology | Tripartite Motif Proteins - metabolism | Muscle, Skeletal - pathology | Ubiquitin-Protein Ligases - genetics | Insulin-Like Growth Factor I - metabolism | Molecular Bases of Disease | SMAD transcription factor | metabolism | muscle atrophy | myostatin | muscle
Journal Article
The Journal of experimental medicine, ISSN 1540-9538, 2010, Volume 207, Issue 11, pp. 2331 - 2341
...− T cells in mice infected with the intestinal helminth Heligmosomoides polygyrus. In vitro, parasite-secreted proteins (termed H... 
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
American Journal of Physiology: Cell Physiology, ISSN 1522-1563, 2009, Volume 296, Issue 6, pp. C1248 - C1257
Loss of muscle mass occurs in a variety of diseases, including cancer, chronic heart failure, aquired immunodeficiency syndrome, diabetes, and renal failure,... 
Myostatin | Muscle atrophy | Akt | Hypertrophy | MYOBLAST DIFFERENTIATION | PHYSIOLOGY | hypertrophy | UBIQUITIN LIGASES | myostatin | CELL BIOLOGY | SKELETAL-MUSCLE | PATHWAY | GROWTH | ATROPHY INVOLVE | MICE | muscle atrophy | EXPRESSION | Phosphorylation | Receptors, Transforming Growth Factor beta - genetics | Age Factors | Muscle Denervation | Male | Muscle, Skeletal - innervation | Muscle, Skeletal - metabolism | Smad3 Protein - metabolism | Proto-Oncogene Proteins c-akt - genetics | Tripartite Motif Proteins | Muscle Development | Muscular Atrophy - physiopathology | Transfection | RNA Interference | Muscle Proteins - metabolism | Cell Differentiation | Muscular Atrophy - prevention & control | Myostatin - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Muscular Atrophy - metabolism | Signal Transduction | Muscular Atrophy - pathology | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Smad2 Protein - metabolism | Ubiquitin-Protein Ligases - metabolism | Mice, Transgenic | Phosphotransferases (Alcohol Group Acceptor) - metabolism | Animals | Carrier Proteins - metabolism | Receptors, Transforming Growth Factor beta - metabolism | Sciatic Nerve - surgery | Muscle, Skeletal - physiopathology | Mice | TOR Serine-Threonine Kinases | Muscle, Skeletal - pathology | Mutation | Transforming Growth Factor beta - metabolism | RNA, Small Interfering - metabolism
Journal Article
The Journal of clinical investigation, ISSN 1558-8238, 2017, Volume 127, Issue 10, pp. 3770 - 3783
.... TGF-beta induces fibroblast activation and differentiation into myofibroblasts that secrete extracellular matrix proteins... 
GENETIC MANIPULATION | MEDICINE, RESEARCH & EXPERIMENTAL | HYPERTROPHY | GROWTH-FACTOR-BETA | HEART-DISEASE | TGF-BETA | SMAD3 | MYOCARDIAL-INFARCTION | IN-VIVO | MYOFIBROBLAST DIFFERENTIATION | PROTECTS | Receptors, Transforming Growth Factor beta - genetics | Heart Diseases - metabolism | Male | Smad3 Protein - metabolism | Myofibroblasts - metabolism | Smad3 Protein - genetics | Gene Deletion | Myocardium - metabolism | Smad2 Protein - genetics | Protein-Serine-Threonine Kinases - metabolism | Myofibroblasts - pathology | Signal Transduction | Protein-Serine-Threonine Kinases - genetics | Smad2 Protein - metabolism | Mice, Transgenic | Myocardium - pathology | Organ Specificity | Myocytes, Cardiac - pathology | Animals | Transforming Growth Factor beta - genetics | Receptors, Transforming Growth Factor beta - metabolism | Fibrosis | Myocytes, Cardiac - metabolism | Mice | Transforming Growth Factor beta - metabolism | Heart Diseases - genetics | Heart Diseases - pathology | Transcription factors | Phosphorylation | Heart attacks | Disease | Homeostasis | Smad3 protein | Gene deletion | Kinases | Proteins | Clonal deletion | Smad2 protein | Rodents | Fibroblasts | Extracellular matrix | Heart diseases | Growth factors | Heart failure | Cytokines | Cardiomyocytes | Gene expression | Pressure | Latency | Adenoviruses | Genetic engineering | Apoptosis
Journal Article