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Science, ISSN 0036-8075, 4/2006, Volume 312, Issue 5770, pp. 117 - 121
Aortic aneurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in the gene that encodes fibrillin-1. Selected... 
Airspace | Receptors | Architecture | Dilatation | Root growth | Placebos | Reports | Mice | Aortic aneurysm | Elastic tissue | Marfan syndrome | PATHOGENESIS | GROWTH-FACTOR-BETA | ACTIVATION | FIBRILLIN | MULTIDISCIPLINARY SCIENCES | RATS | RECEPTOR | SMOOTH-MUSCLE-CELLS | BLOCKADE | CONTRIBUTES | DILATATION | Angiotensin II Type 1 Receptor Blockers - therapeutic use | Propranolol - therapeutic use | Neutralization Tests | Aortic Aneurysm - etiology | Lung Diseases - drug therapy | Marfan Syndrome - drug therapy | Propranolol - administration & dosage | Antibodies - immunology | Transforming Growth Factor beta - antagonists & inhibitors | Female | Marfan Syndrome - complications | Microfilament Proteins - genetics | Adrenergic beta-Antagonists - administration & dosage | Adrenergic beta-Antagonists - therapeutic use | Angiotensin II Type 1 Receptor Blockers - administration & dosage | Aortic Aneurysm - prevention & control | Disease Models, Animal | Transforming Growth Factor beta - immunology | Fibrillin-1 | Lung - pathology | Pulmonary Alveoli - pathology | Signal Transduction | Fibrillins | Pregnancy Complications - drug therapy | Aorta - pathology | Pregnancy | Elastic Tissue - pathology | Animals | Receptor, Angiotensin, Type 1 - metabolism | Losartan - therapeutic use | Marfan Syndrome - metabolism | Marfan Syndrome - pathology | Losartan - administration & dosage | Lung Diseases - pathology | Mutation | Transforming Growth Factor beta - metabolism | Complications and side effects | Aortic aneurysms | Genetic aspects | Research | Risk factors
Journal Article
Kidney International, ISSN 0085-2538, 05/2012, Volume 81, Issue 9, pp. 865 - 879
Inflammation is recognized as an important contributor to lymphangiogenesis; however, in tubulointerstitial lesions in human chronic kidney diseases, this... 
TGF-β | tubular epithelial cells | podoplanin | LYVE-1 | TGF-b | LYMPHATIC VESSELS | TGF-BETA-1 MESSENGER-RNA | METASTASIS | MACROPHAGES | VEGF-C | MECHANISMS | RENAL FIBROSIS | TGF-beta | INFLAMMATION | UROLOGY & NEPHROLOGY | PULMONARY-FIBROSIS | Kidney Tubules - physiopathology | Up-Regulation | Membrane Glycoproteins - metabolism | Humans | Transforming Growth Factor beta1 - metabolism | Male | Ureteral Obstruction - metabolism | RNA, Messenger - metabolism | Time Factors | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Ureteral Obstruction - genetics | Kidney Tubules - pathology | Kidney Tubules - metabolism | Real-Time Polymerase Chain Reaction | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Fibroblasts - metabolism | Pyrazoles - pharmacology | Cell Line | Kidney Tubules - drug effects | Signal Transduction | Rats | Receptors, Cell Surface - metabolism | Transforming Growth Factor beta1 - genetics | Reverse Transcriptase Polymerase Chain Reaction | Rats, Sprague-Dawley | Ureteral Obstruction - physiopathology | Vascular Endothelial Growth Factor C - genetics | Membrane Glycoproteins - genetics | Lymphangiogenesis - drug effects | Macrophages - metabolism | Pyrroles - pharmacology | Animals | Receptors, Transforming Growth Factor beta - antagonists & inhibitors | Receptors, Transforming Growth Factor beta - metabolism | Vascular Endothelial Growth Factor C - metabolism | Ureteral Obstruction - pathology | Fibrosis | Mice | Receptors, Cell Surface - genetics
Journal Article
Hepatology, ISSN 0270-9139, 10/2009, Volume 50, Issue 4, pp. 1140 - 1151
Journal Article
Cell, ISSN 0092-8674, 03/2018, Volume 173, Issue 1, pp. 104 - 116.e12
Human diseases are often caused by loss of somatic cells that are incapable of re-entering the cell cycle for regenerative repair. Here, we report a... 
heart failure | cyclin | proliferation | cell cycle | regeneration | cytokinesis | cardiomyocyte | cell division | CDK | heart | HYPERTROPHY | INFARCTION | EXPRESSION ANALYSIS | AMPLIFICATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MICE | ZEBRAFISH HEART REGENERATION | FAILURE | CANCER | FIBROBLASTS | PROGRAM | CELL BIOLOGY | Cyclin D1 - metabolism | Cell Proliferation | Protein-Tyrosine Kinases - metabolism | Cyclin-Dependent Kinase 4 - genetics | Heart - physiology | Humans | Myosin Heavy Chains - genetics | Cyclin B1 - metabolism | CDC2 Protein Kinase - metabolism | Cell Cycle Proteins - antagonists & inhibitors | Myocardial Infarction - pathology | Transforming Growth Factor beta - antagonists & inhibitors | Myocardial Infarction - veterinary | Induced Pluripotent Stem Cells - cytology | Induced Pluripotent Stem Cells - metabolism | CDC2 Protein Kinase - genetics | Myocytes, Cardiac - cytology | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Cyclin B1 - genetics | Rats | Mice, Transgenic | Nuclear Proteins - metabolism | Myocardial Infarction - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Cytokinesis | Regeneration | Animals | Cyclin D1 - genetics | Nuclear Proteins - antagonists & inhibitors | Myocytes, Cardiac - metabolism | Mice | Transforming Growth Factor beta - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Heart | Bone morphogenetic proteins | Transforming growth factors | Cell cycle | Stem cells | Cell Cycle | Cardiomyocyte | Cell Division | Cyclin
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 04/2017, Volume 76, Issue 4, pp. 756 - 764
ObjectivesHedgehog signalling plays a critical role during the pathogenesis of fibrosis in systemic sclerosis (SSc). Besides canonical hedgehog signalling with... 
Fibroblasts | Systemic Sclerosis | Treatment | EXPERIMENTAL FIBROSIS | TGF-BETA | INHIBITION | SONIC HEDGEHOG | KIDNEY FIBROSIS | PATHWAY | DISEASE | RHEUMATOLOGY | STELLATE CELL ACTIVATION | SYSTEMIC-SCLEROSIS | CANCER | Receptors, Transforming Growth Factor beta - genetics | Humans | Middle Aged | Zinc Finger Protein Gli2 | Hedgehog Proteins - metabolism | Male | Smad3 Protein - metabolism | RNA, Messenger - metabolism | Young Adult | Collagen Type I - genetics | Kruppel-Like Transcription Factors - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Adult | Female | Pulmonary Fibrosis - metabolism | Plasminogen Activator Inhibitor 1 - genetics | Smoothened Receptor - antagonists & inhibitors | Skin - pathology | Fibroblasts - metabolism | Pteridines - pharmacology | Scleroderma, Systemic - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Scleroderma, Systemic - genetics | Mice, Transgenic | Pyrimidines - pharmacology | Recombinant Proteins - pharmacology | Gene Knockout Techniques | Mice, Knockout | Transforming Growth Factor beta - pharmacology | Animals | Receptors, Transforming Growth Factor beta - antagonists & inhibitors | Signal Transduction - drug effects | Fibroblasts - drug effects | Anilides - pharmacology | Fibrosis | Pulmonary Fibrosis - chemically induced | Aged | Connective Tissue Growth Factor - genetics | Mice | Pyridines - pharmacology | Kruppel-Like Transcription Factors - antagonists & inhibitors | Kruppel-Like Transcription Factors - genetics | Transforming Growth Factor beta - metabolism | Skin - drug effects | Transcription factors | Research | Systemic scleroderma | Transforming growth factors | Scleroderma (Disease)
Journal Article
Journal Article
Cancer Letters, ISSN 0304-3835, 2016, Volume 379, Issue 2, pp. 166 - 172
Journal Article
Journal Article
Journal Article
Molecular Cancer Therapeutics, ISSN 1535-7163, 04/2008, Volume 7, Issue 4, pp. 829 - 840
Most pancreatic cancer patients present with inoperable disease or develop metastases after surgery. Conventional therapies are usually ineffective in treating... 
anoikis | TGF-β | pancreatic cancer | experimental therapeutics | metastasis | BREAST-CANCER | PULMONARY | INVASION | TGF-BETA | ENHANCED EXPRESSION | CARCINOMA CELLS | ONCOLOGY | PHENOTYPE | KINASE INHIBITOR | DECREASED SURVIVAL | TUMORIGENESIS | Pancreatic Neoplasms - metabolism | Apoptosis - drug effects | Humans | Lung Neoplasms - metabolism | Neovascularization, Pathologic | Deoxycytidine - pharmacology | Pancreatic Neoplasms - drug therapy | Lung Neoplasms - secondary | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Antimetabolites, Antineoplastic - pharmacology | Phosphorylation - drug effects | Tumor Cells, Cultured | Drug Therapy, Combination | Protein-Serine-Threonine Kinases - metabolism | Pyrazoles - pharmacology | Signal Transduction | Neoplasm Invasiveness | Mice, Inbred C57BL | Pancreatic Neoplasms - pathology | Smad2 Protein - metabolism | Survival Rate | Xenograft Model Antitumor Assays | Cell Movement - drug effects | Pyrroles - pharmacology | Animals | Receptors, Transforming Growth Factor beta - antagonists & inhibitors | Lung Neoplasms - prevention & control | Receptors, Transforming Growth Factor beta - metabolism | Mice, Nude | Ribonucleotide Reductases - antagonists & inhibitors | Anoikis - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Transforming Growth Factor beta - metabolism | Deoxycytidine - analogs & derivatives | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 10, p. e26514
The transcriptional repressors Snail and Slug are situated at the core of several signaling pathways proposed to mediate epithelial to mesenchymal transition... 
TGF-BETA | PROTEIN | CLAUDIN-LOW | MULTIDISCIPLINARY SCIENCES | REPRESSES E-CADHERIN | GENE-EXPRESSION | SUPERFAMILY | OVARIAN | TGF-BETA-PAR6 POLARITY PATHWAY | EPITHELIAL-MESENCHYMAL TRANSITIONS | FIBROBLASTS | Transcription, Genetic - drug effects | Receptors, Transforming Growth Factor beta - genetics | Humans | Genetic Loci - genetics | Substrate Specificity | Epithelial-Mesenchymal Transition - drug effects | Mammary Glands, Human - metabolism | RNA, Messenger - metabolism | Breast Neoplasms - metabolism | Dioxoles - pharmacology | Transforming Growth Factor beta - antagonists & inhibitors | Female | Benzamides - pharmacology | Snail Family Transcription Factors | Mammary Glands, Human - drug effects | Pyrazoles - pharmacology | RNA, Messenger - genetics | Intercellular Junctions - metabolism | Protein-Serine-Threonine Kinases - genetics | Mammary Glands, Human - pathology | Transcription Factors - genetics | Down-Regulation - drug effects | Transcription Factors - metabolism | Cell Movement - drug effects | Acetylation - drug effects | Phenotype | Pyrroles - pharmacology | Breast Neoplasms - genetics | Signal Transduction - drug effects | Breast Neoplasms - pathology | Cell Differentiation - drug effects | Intercellular Junctions - drug effects | Cell Line, Tumor | Histones - metabolism | Transforming Growth Factor beta - metabolism | Analysis | Genes | Stem cells | Bone morphogenetic proteins | Breast cancer | DNA binding proteins | Metastasis | Transforming growth factors | Health sciences | Transcription factors | Leukocyte migration | Mesenchyme | Laboratories | Epithelial cells | Transforming growth factor-b | Cytology | Kinases | Metastases | Morphogenesis | Proteins | Signal transduction | Pathways | Repressors | Cell cycle | Acetylation | Growth factors | Invasiveness | Environmental health | Gene expression | Ribonucleic acid--RNA | Signaling | DNA microarrays | Collaboration | Medical prognosis | Adenoviruses | Breast | Snail protein | Cell migration | Cancer | Tumors | RNA | Ribonucleic acid
Journal Article