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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
Nature biotechnology, ISSN 1546-1696, 2002, Volume 20, Issue 6, pp. 619 - 622
Journal Article
Molecular and Cellular Biology, ISSN 0270-7306, 07/2012, Volume 32, Issue 14, pp. 2904 - 2916
Journal Article
The 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
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, 2011, Volume 6, Issue 7, p. e21796
... 1 , Jae-Yong Lee 1 , SungChan Kim 1 , Mae Ja Park 3 , Zigang Dong 2 , Jaebong Kim 1 , * Introduction AP-1 (activator protein-1) protein is an evolutionarily... 
TGF-BETA | FGF | BIOLOGY | FIBROBLAST-GROWTH-FACTOR | CELL-PROLIFERATION | BMP-4 | SPECIFICATION | EARLY XENOPUS DEVELOPMENT | TUMORIGENESIS | EMBRYOS | MESODERM INDUCTION | Embryo, Nonmammalian - cytology | Immunoprecipitation | Luciferases - metabolism | Xenopus Proteins - genetics | Transcription Factor AP-1 - genetics | Bone Morphogenetic Protein 4 - genetics | Protein Multimerization | Transcriptional Activation | Embryo, Nonmammalian - metabolism | Glycoproteins - metabolism | Activins - metabolism | Smad3 Protein - metabolism | Bone Morphogenetic Protein 4 - metabolism | Transcription Factor AP-1 - metabolism | Goosecoid Protein - genetics | Goosecoid Protein - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Smad3 Protein - genetics | In Situ Hybridization | Chromatin Immunoprecipitation | Glycoproteins - genetics | Promoter Regions, Genetic | Signal Transduction | Proto-Oncogene Proteins c-jun - genetics | RNA, Messenger - genetics | Xenopus laevis | Gene Expression Regulation | Intercellular Signaling Peptides and Proteins - genetics | Proto-Oncogene Proteins c-fos - metabolism | Reverse Transcriptase Polymerase Chain Reaction | T-Box Domain Proteins - genetics | Blotting, Western | T-Box Domain Proteins - metabolism | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Proto-Oncogene Proteins c-jun - metabolism | Organizers, Embryonic - metabolism | Protein Binding | Proto-Oncogene Proteins c-fos - genetics | Xenopus Proteins - metabolism | Activins - genetics | Physiological aspects | Gene expression | Bone morphogenetic proteins | Fibroblast growth factor | Transcription factors | Transcription | Genes | Gene regulation | Biochemistry | Smad3 protein | Reptiles & amphibians | Proteins | Embryogenesis | Physiology | Growth factors | c-Fos protein | Bone morphogenetic protein 4 | Cytokines | Activator protein 1 | c-Jun protein | Chordin | Noggin protein | Embryos | Mutants | Embryonic growth stage | Medicine | Signaling | Stem cells | Activin | Binding sites
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
PloS one, ISSN 1932-6203, 2015, Volume 10, Issue 3, pp. e0120045 - e0120045
Cervical cancer is the major cause of cancer related deaths in women, especially in developing countries and Human Papilloma Virus infection in conjunction... 
EPITHELIAL-MESENCHYMAL TRANSITION | BREAST-CANCER | MIGRATION | APOPTOSIS | GROWTH-FACTOR-BETA | ACTIVATION | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | MECHANISMS | HUMAN-PAPILLOMAVIRUS | TRANSCRIPTION FACTOR | Receptors, Transforming Growth Factor beta - genetics | Humans | Collagen - chemistry | Epithelial-Mesenchymal Transition - drug effects | Wnt Proteins - metabolism | Smad4 Protein - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Peptidylprolyl Isomerase - metabolism | Peptidylprolyl Isomerase - genetics | Protein-Serine-Threonine Kinases - metabolism | Emodin - pharmacology | Curcumin - pharmacology | Cyclin-Dependent Kinase Inhibitor p21 - antagonists & inhibitors | Smad3 Protein - antagonists & inhibitors | beta Catenin - metabolism | Drug Synergism | Cell Movement - drug effects | Receptors, Transforming Growth Factor beta - antagonists & inhibitors | Cyclin D1 - genetics | Signal Transduction - drug effects | Cell Line, Tumor | Laminin - chemistry | HeLa Cells | Cyclin D1 - metabolism | Smad4 Protein - antagonists & inhibitors | Gene Expression Regulation, Neoplastic | Smad3 Protein - metabolism | Proteoglycans - chemistry | Smad3 Protein - genetics | Cyclin D1 - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Wnt Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Transforming Growth Factor beta - antagonists & inhibitors | Female | Snail Family Transcription Factors | Protein-Serine-Threonine Kinases - genetics | Transcription Factors - antagonists & inhibitors | NIMA-Interacting Peptidylprolyl Isomerase | Transcription Factors - genetics | Smad4 Protein - metabolism | beta Catenin - genetics | Transcription Factors - metabolism | Transforming Growth Factor beta - genetics | Receptors, Transforming Growth Factor beta - metabolism | beta Catenin - antagonists & inhibitors | Cell Proliferation - drug effects | Antineoplastic Agents, Phytogenic - pharmacology | Transforming Growth Factor beta - metabolism | Drug Combinations | Biotechnology | Deregulation | Wnt protein | Mesenchyme | Downstream effects | Crosstalk | Viruses | Smad3 protein | Biochemistry | Metastasis | Kinases | Pin1 protein | Cancer therapies | Carcinogenesis | Smad4 protein | Developing countries--LDCs | Cell adhesion & migration | Proteins | β-catenin | Signal transduction | Carcinogens | Pathways | Cell cycle | Curcumin | Tumorigenesis | Inhibition | Downstream | Medical research | Breast cancer | Tumor cell lines | Gene expression | Cervix | Emodin | Signaling | Chemotherapy | Phytochemicals | Ligands | Cell migration | Cervical cancer | Cancer | Apoptosis | Index Medicus | Developing countries | LDCs
Journal Article
Science translational medicine, ISSN 1946-6242, 2016, Volume 8, Issue 348, pp. 348ra98 - 348ra98
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