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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 | Abdominal surgery | Musculoskeletal system | Signal transduction | Cell growth | Kinases | Gene expression | Cells | Index Medicus
Journal Article
Nucleic Acids Research, ISSN 0305-1048, 09/2018, Volume 46, Issue 17, pp. 9220 - 9235
Journal Article
Scientific Reports, ISSN 2045-2322, 12/2018, Volume 8, Issue 1, pp. 998 - 10
Radiation-induced lung injury has restricted radiotherapy for thoracic cancer. The purpose of this study was to investigate the radioprotective effects of... 
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 | 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 | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 10/2010, Volume 107, Issue 43, pp. 18404 - 18409
Journal Article
Cellular and Molecular Life Sciences, ISSN 1420-682X, 7/2018, Volume 75, Issue 14, pp. 2663 - 2680
Primary cilia are sensory organelles that coordinate multiple cellular signaling pathways, including Hedgehog (HH), Wingless/Int (WNT) and Transforming Growth... 
Biomedicine, general | Biochemistry, general | TSC | LC3b | Primary cilia | TGF-β signaling | WNT5a | Hedgehog signaling | Autophagy | Cell Biology | Life Sciences | Life Sciences, general | mTOR | GLI1 EXPRESSION | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | PROTEIN-COUPLED RECEPTORS | CELL-SIZE | CELL BIOLOGY | TSC1-TSC2 COMPLEX | TGF-beta signaling | GROWTH-FACTOR-BETA | MEDIATORS | Tumor Suppressor Proteins - metabolism | Signal Transduction | Cells, Cultured | Gene Expression Regulation | Hedgehog Proteins - metabolism | Smoothened Receptor - metabolism | Smoothened Receptor - genetics | Cilia - metabolism | Mice, Knockout | Zinc Finger Protein Gli2 - metabolism | Animals | Tuberous Sclerosis Complex 2 Protein | Hedgehog Proteins - genetics | RNA Interference | Embryo, Mammalian - cytology | Tumor Suppressor Proteins - genetics | Tuberous Sclerosis Complex 1 Protein | Zinc Finger Protein Gli2 - genetics | Fibroblasts - metabolism | Tuberous sclerosis | Bone morphogenetic proteins | Protein biosynthesis | Molecular genetics | Transforming growth factors | TOR protein | Tuberous sclerosis 2 protein | Phosphorylation | Wnt protein | Transforming growth factor | Hamartin | Kinases | TSC1 protein | Sclerosis | Proteins | Signal transduction | Smad2 protein | Fibroblasts | Elongation | Cilia | Phenotypes | Rapamycin | Embryo fibroblasts | Organelles | Embryos | TSC2 protein | Signaling | Protein synthesis | Hedgehog protein | Dismantling | Index Medicus | Original
Journal Article
Endocrinology, ISSN 0013-7227, 05/2014, Volume 155, Issue 5, pp. 1970 - 1981
FSH is an essential regulator of mammalian reproduction. Its synthesis by pituitary gonadotrope cells is regulated by multiple endocrine and paracrine factors,... 
PATHWAYS | GROWTH-FACTOR-BETA | ACTIVATION | ACTIVIN-A INDUCTION | TGF-BETA | L45 LOOP | II RECEPTOR | TRANSCRIPTION | KINASE | ENDOCRINOLOGY & METABOLISM | HORMONE BETA-SUBUNIT | Phosphorylation | Humans | Activins - antagonists & inhibitors | Activins - metabolism | Gonadotrophs - metabolism | Smad3 Protein - metabolism | Smad2 Protein - antagonists & inhibitors | Smad3 Protein - genetics | Bone Morphogenetic Protein 2 - metabolism | Smad2 Protein - genetics | Follicle Stimulating Hormone, beta Subunit - metabolism | Bone Morphogenetic Protein Receptors, Type I - agonists | Transcription, Genetic | Follicle Stimulating Hormone, beta Subunit - biosynthesis | Genes, Reporter | Bone Morphogenetic Protein Receptors, Type I - antagonists & inhibitors | Recombinant Proteins - metabolism | Bone Morphogenetic Protein 2 - agonists | Bone Morphogenetic Protein 2 - genetics | Cell Line | Signal Transduction | Bone Morphogenetic Protein 2 - antagonists & inhibitors | Gene Silencing | Smad2 Protein - metabolism | Bone Morphogenetic Protein Receptors, Type I - genetics | Recombinant Proteins - chemistry | Bone Morphogenetic Protein Receptors, Type I - metabolism | Smad3 Protein - antagonists & inhibitors | Animals | Follicle Stimulating Hormone, beta Subunit - genetics | Mice | Protein Processing, Post-Translational | RNA, Small Interfering | Index Medicus | Abridged Index Medicus
Journal Article
Nature Cell Biology, ISSN 1465-7392, 11/2014, Volume 16, Issue 12, pp. 1257 - 1264
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2012, Volume 7, Issue 5, pp. e36964 - e36964
Articular cartilage is physiologically exposed to repeated loads. The mechanical properties of cartilage are due to its extracellular matrix, and homeostasis... 
DISTURBED FLOW | GROWTH-FACTOR-BETA | IN-VITRO | TGF-BETA | BOVINE ARTICULAR CHONDROCYTES | MULTIDISCIPLINARY SCIENCES | ENDOTHELIAL-CELLS | SHEAR-STRESS | MECHANICAL STIMULATION | CARTILAGE TISSUE | 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 | Index Medicus | 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
Journal of Biological Chemistry, ISSN 0021-9258, 01/2014, Volume 289, Issue 3, pp. 1788 - 1797
Journal Article
JOURNAL OF BIOLOGICAL CHEMISTRY, ISSN 0021-9258, 10/2018, Volume 293, Issue 41, pp. 15867 - 15886
Transforming growth factor-beta (TGF beta) signaling through SMAD2/3 is an important driver of pathological fibrosis in multiple organ systems. TGF signaling... 
TGF-BETA | INTEGRAL PROTEIN | SMAD PROTEINS | mechanotransduction | BIOCHEMISTRY & MOLECULAR BIOLOGY | MEMBRANE PROTEIN | Buschke-Ollendorff syndrome | LEMD3 | actin | IN-VITRO | MAN1 | LEM | pulmonary fibrosis | SMAD transcription factor | transforming growth factor (TGF-) | nuclear lamina | LATENT TGF-BETA-1 | EXTRACELLULAR-MATRIX | BUSCHKE-OLLENDORFF-SYNDROME | IDIOPATHIC PULMONARY-FIBROSIS | nuclear membrane | NONSENSE MUTATION | Phosphorylation | Mechanotransduction, Cellular - drug effects | Protein Phosphatase 2C - metabolism | Humans | Actins - metabolism | Extracellular Matrix - metabolism | Smad3 Protein - metabolism | Smad2 Protein - antagonists & inhibitors | Idiopathic Pulmonary Fibrosis - metabolism | Smad2 Protein - chemistry | Nuclear Lamina - metabolism | Transforming Growth Factor beta - antagonists & inhibitors | Lung - metabolism | Membrane Proteins - metabolism | Fibroblasts - metabolism | Peptide Fragments - metabolism | Smad2 Protein - metabolism | Nuclear Proteins - metabolism | Nuclear Proteins - chemistry | Smad3 Protein - antagonists & inhibitors | Peptide Fragments - chemistry | Membrane Proteins - antagonists & inhibitors | Membrane Proteins - chemistry | Nuclear Proteins - antagonists & inhibitors | Cytosol - metabolism | Smad3 Protein - chemistry | Transforming Growth Factor beta - metabolism | Index Medicus
Journal Article
Biochemical Journal, ISSN 0264-6021, 03/2005, Volume 386, Issue 3, pp. 461 - 470
Inhibitory Smad, Smad7, is a potent inhibitor of TGF-beta (transforming growth factor-beta) superfamily signalling. By binding to activated type I receptors,... 
Developmentally down-regulated 4-2 (NEDD4-2) | Bone morphogenetic protein (BMP) | Smad | Neural precursor cell expressed | Homologous to the E6-accessory protein C-terminus (HECT) | Transforming growth factor-β (TGF-β) | Humans | Protein-Serine-Threonine Kinases | Ubiquitin - metabolism | Cytoplasm - metabolism | RNA, Messenger - metabolism | DNA-Binding Proteins - metabolism | Bone Morphogenetic Proteins - metabolism | Cell Nucleus - metabolism | Trans-Activators - genetics | Nedd4 Ubiquitin Protein Ligases | Transcription, Genetic | Proto-Oncogene Proteins - metabolism | Smad7 Protein | Cell Line | Signal Transduction | Smad6 Protein | Endosomal Sorting Complexes Required for Transport | RNA, Messenger - genetics | Ubiquitin-Protein Ligases - metabolism | Intracellular Signaling Peptides and Proteins | Activin Receptors, Type I - metabolism | DNA-Binding Proteins - genetics | Protein Transport | Two-Hybrid System Techniques | Smad3 Protein | Animals | Receptors, Transforming Growth Factor beta - metabolism | Cell Line, Tumor | Protein Binding | Ligands | Trans-Activators - metabolism | Mice | Ubiquitin-Protein Ligases - genetics | Transforming Growth Factor beta - metabolism | Smad2 Protein | Index Medicus | BMPR-IB, BMP type IB receptor | TβR-I, transforming growth factor-β type I receptor | developmentally down-regulated 4-2 (NEDD4-2) | Ski-related novel protein N (SnoN) | I-Smad, inhibitory Smad | transforming growth factor-β (TGF-β) | homologous to the E6-accessory protein C-terminus (HECT) | R-Smad, receptor-regulated Smad | SnoN, Ski-related novel protein N | RING, really interesting new gene | F-box protein | bone morphogenetic protein (BMP) | ROC1, regulator of Cullins 1 | HECT, homologous to the E6-accessory protein C-terminus | siRNA, small interfering RNA | NEDD4-2, neural precursor cell expressed, developmentally down-regulated 4-2 | SCF, Skp1 | neural precursor cell expressed | Smurf, Smad ubiquitin regulatory factor | TGF-β, transforming growth factor-β | Cullin1 | BMP, bone morphogenetic protein | Co-Smad, common-partner Smad
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2014, Volume 9, Issue 5, pp. e96365 - e96365
Epithelial-mesenchymal transition (EMT) of retinal pigment epithelium (RPE) cells is a major pathologic change in the development of proliferative... 
FIBROSIS | PROLIFERATIVE VITREORETINAL DISEASES | ACTIVATION | TISSUE GROWTH-FACTOR | FACTOR-BETA | MULTIDISCIPLINARY SCIENCES | INVOLVEMENT | KINASE | SMAD | INHIBITOR | EXPRESSION | Epithelial Cells - metabolism | Gene Expression - drug effects | Nitriles - pharmacology | Receptors, Notch - metabolism | Epithelial Cells - drug effects | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Epithelial-Mesenchymal Transition - drug effects | Receptors, Notch - genetics | Smad3 Protein - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Multiprotein Complexes - metabolism | Serrate-Jagged Proteins | Dioxoles - pharmacology | Benzamides - pharmacology | Membrane Proteins - metabolism | Jagged-1 Protein | Calcium-Binding Proteins - metabolism | Cell Line | Butadienes - pharmacology | Membrane Proteins - genetics | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Intercellular Signaling Peptides and Proteins - genetics | Smad2 Protein - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Transforming Growth Factor beta2 - pharmacology | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Signal Transduction - drug effects | Receptor, Notch3 | Smad Proteins - metabolism | Retinal Pigment Epithelium - cytology | Calcium-Binding Proteins - genetics | Mitogen-Activated Protein Kinase 1 - metabolism | Smad protein | Mesenchyme | Laboratories | Transforming growth factor | Retina | Activation | Kinases | Carcinogenesis | Fibronectin | Retinal pigment epithelium | Metastases | Signal transduction | Carcinogens | N-Cadherin | Pathways | Breakdowns | Smad2 protein | Collagen (type IV) | Growth factors | Visually handicapped people | Immunoglobulins | Cytokines | Medical treatment | Extracellular signal-regulated kinase | Epithelium | Cadherin | Trauma | Signaling | Inhibitors | Fibrosis | Notch protein | Cancer | Index Medicus
Journal Article