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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
Proceedings of the National Academy of Sciences - PNAS, ISSN 0027-8424, 10/2010, Volume 107, Issue 43, pp. 18404 - 18409
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
Trends in immunology, ISSN 1471-4906, 2004, Volume 25, Issue 10, pp. 513 - 517
Journal Article
PloS one, ISSN 1932-6203, 09/2011, Volume 6, Issue 9, p. e25021
Background: Hub proteins are connected through binding interactions to many other proteins... 
TRANSCRIPTION FACTORS | BREAST-CANCER | TGF-BETA | MYOGENIC DIFFERENTIATION | EPITHELIAL-CELLS | STRUCTURAL BASIS | CRYSTAL-STRUCTURE | BIOLOGY | BETA SIGNAL-TRANSDUCTION | TRANSFORMING-GROWTH-FACTOR | MESENCHYMAL TRANSITION | Cell Proliferation | Luciferases - metabolism | Oligonucleotide Array Sequence Analysis | Humans | Gene Expression Profiling | Smad3 Protein - metabolism | Immunoenzyme Techniques | DNA-Binding Proteins - metabolism | Smad3 Protein - genetics | Kidney - metabolism | Myoblasts - metabolism | Smad4 Protein - genetics | Smad2 Protein - genetics | Myoblasts - cytology | Protein Interaction Domains and Motifs | Real-Time Polymerase Chain Reaction | Biomarkers - metabolism | Proto-Oncogene Proteins - metabolism | Signal Transduction | RNA, Messenger - genetics | Trans-Activators | Cells, Cultured | Gene Expression Regulation | Smad2 Protein - metabolism | Ubiquitin-Protein Ligases - metabolism | Models, Molecular | Proto-Oncogene Proteins - genetics | Kidney - cytology | DNA-Binding Proteins - genetics | Mutation - genetics | Reverse Transcriptase Polymerase Chain Reaction | Nerve Tissue Proteins - genetics | Smad4 Protein - metabolism | Blotting, Western | Nerve Tissue Proteins - metabolism | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Transforming Growth Factor beta - genetics | Protein Conformation | Smad3 Protein - chemistry | Mice | Ubiquitin-Protein Ligases - genetics | Transforming Growth Factor beta - metabolism | Amino acids | Bone morphogenetic proteins | Cellular signal transduction | Genetic aspects | Binding proteins | Transforming growth factors | Gene expression | Protein-protein interactions | Protein binding | Transcription factors | Laboratories | Genes | Transforming growth factor-b | Oncology | Smad3 protein | Kinases | Smad4 protein | Proteins | Signal transduction | Cell growth | Reporter gene | Cooperation | Spots | Interleukin 1 | Stress response | Growth factors | Public health | Binding | Medical research | Interleukin 11 | Gelatinase B | Mutants | Medicine | Signaling | Mutagenesis | Lymphomas | Mutation | Protein interaction | Binding sites | Cancer | Apoptosis | Transduction
Journal Article
PloS one, ISSN 1932-6203, 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 | Disabled people | 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 | Immunoglobulins | Cytokines | Medical treatment | Extracellular signal-regulated kinase | Epithelium | Cadherin | Trauma | Signaling | Inhibitors | Fibrosis | Notch protein | Cancer | Index Medicus
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 (London), ISSN 1476-4687, 2004, Volume 431, Issue 7005, pp. 205 - 211
... signalling proteins Smad2 and Smad3, as well as impaired induction of TGF-β target genes. Expression of cytoplasmic Pml is induced by TGF-β... 
CANCER-CELLS | ANDROGEN RECEPTOR | PREMATURE SENESCENCE | ONCOGENIC RAS | MONOCYTIC DIFFERENTIATION | TUMOR SUPPRESSION | MULTIDISCIPLINARY SCIENCES | GROWTH | ALPHA | PROTEIN ISOFORMS | ACUTE PROMYELOCYTIC LEUKEMIA | Transcription, Genetic - drug effects | Oncogene Proteins, Fusion - metabolism | Leukemia, Promyelocytic, Acute - pathology | Apoptosis - drug effects | Humans | Transcription Factors - deficiency | Cellular Senescence - drug effects | Cytoplasm - metabolism | Neoplasm Proteins - metabolism | Endosomes - metabolism | DNA-Binding Proteins - metabolism | Leukemia, Promyelocytic, Acute - metabolism | Nuclear Proteins - deficiency | Endosomes - drug effects | Trans-Activators - genetics | Fibroblasts | Neoplasm Proteins - genetics | Nuclear Proteins - genetics | Cell Line | B-Lymphocytes - cytology | Nuclear Proteins - metabolism | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Mutation - genetics | Cell Division - drug effects | Protein Transport | Transcription Factors - metabolism | B-Lymphocytes - drug effects | Carrier Proteins - genetics | Transforming Growth Factor beta - pharmacology | Smad3 Protein | Animals | Carrier Proteins - metabolism | Receptors, Transforming Growth Factor beta - metabolism | Signal Transduction - drug effects | Cell Line, Tumor | Protein Binding | Trans-Activators - metabolism | Mice | Neoplasm Proteins - deficiency | Cytoplasm - drug effects | Promyelocytic Leukemia Protein | Tumor Suppressor Proteins | Smad2 Protein | Cytokines | Leukemia | Tumors | Cancer
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