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Nature communications, ISSN 2041-1723, 2019, Volume 10, Issue 1, pp. 3616 - 19
.... Here, we use systems genetics to identify a pro-fibrotic gene network in the diseased heart and show that this network is regulated by the E3 ubiquitin ligase WWP2, specifically by the WWP2-N terminal isoform... 
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
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 | Transduction | Mutation | Protein interaction | Binding sites | Cancer | Apoptosis
Journal Article
Nature cell biology, ISSN 1476-4679, 2014, Volume 16, Issue 12, pp. 1257 - 1264
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
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
Nucleic Acids Research, ISSN 0305-1048, 09/2018, Volume 46, Issue 17, pp. 9220 - 9235
Journal Article
The Journal of experimental medicine, ISSN 1540-9538, 2010, Volume 207, Issue 8, pp. 1589 - 1597
Uncontrolled extracellular matrix production by fibroblasts in response to tissue injury contributes to fibrotic diseases, such as idiopathic pulmonary... 
MEDICINE, RESEARCH & EXPERIMENTAL | PHOSPHATASE | MECHANISMS | GROWTH-FACTOR | IMMUNOLOGY | MYOFIBROBLAST DIFFERENTIATION | EXPRESSION | MICRORNA | Oligonucleotides - genetics | Pulmonary Fibrosis - therapy | Idiopathic Pulmonary Fibrosis - genetics | Gene Expression - drug effects | Gene Expression - genetics | Humans | Actins - metabolism | MicroRNAs - metabolism | Pulmonary Fibrosis - genetics | Idiopathic Pulmonary Fibrosis - metabolism | Actins - genetics | Antisense Elements (Genetics) - therapeutic use | Collagen - genetics | Lung - metabolism | Phosphorylation - drug effects | Smad7 Protein - genetics | Extracellular Matrix Proteins - metabolism | Transforming Growth Factor beta1 - pharmacology | Fibroblasts - metabolism | Smad7 Protein - metabolism | Cell Line | Lung - pathology | Extracellular Matrix Proteins - genetics | Mice, Inbred C57BL | Smad2 Protein - metabolism | Mice, Transgenic | Pulmonary Fibrosis - pathology | Transforming Growth Factor beta1 - genetics | Fibroblasts - pathology | Fibronectins - metabolism | Collagen - metabolism | Animals | Fibroblasts - drug effects | Antisense Elements (Genetics) - genetics | Idiopathic Pulmonary Fibrosis - pathology | Pulmonary Fibrosis - chemically induced | Bleomycin - pharmacology | Fibronectins - genetics | Mice | MicroRNAs - genetics | Brief Definitive Report
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
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