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81. Full Text Losartan, an AT1 Antagonist Prevents Aortic Aneurysm in a Mouse Model of Marfan Syndrome
by Jennifer P. Habashi and Daniel P. Judge and Tammy M. Holm and Ronald D. Cohn and Bart L. Loeys and Timothy K. Cooper and Loretha Myers and Erin C. Klein and Guosheng Liu and Carla Calvi and Megan Podowski and Enid R. Neptune and Marc K. Halushka and Djahida Bedja and Kathleen Gabrielson and Daniel B. Rifkin and Luca Carta and Francesco Ramirez and David L. Huso and Harry C. Dietz
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
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82. Full Text Transforming growth factor-β induces vascular endothelial growth factor-C expression leading to lymphangiogenesis in rat unilateral ureteral obstruction
by Suzuki, Yasuhiro and Ito, Yasuhiko and Mizuno, Tomohiro and Mizuno, Masashi and Kinashi, Hiroshi and Sawai, Akiho and Noda, Yukihiro and Shimizu, Hideaki and Fujita, Yoshiro and Matsui, Katsuyuki and Maruyama, Shoichi and Imai, Enyu and Matsuo, Seiichi and Takei, Yoshifumi
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
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83. Full Text Inhibition of transforming growth factor β receptor I kinase blocks hepatocellular carcinoma growth through neo‐angiogenesis regulation
by Mazzocca, Antonio and Fransvea, Emilia and Lavezzari, Gabriela and Antonaci, Salvatore and Giannelli, Gianluigi
Hepatology, ISSN 0270-9139, 10/2009, Volume 50, Issue 4, pp. 1140 - 1151
Curative therapies for patients with hepatocellular carcinoma (HCC) are mainly invasive, and with the exception of sorafenib, no medical treatments are... 
MIGRATION | TRIAL | CELLS | BEVACIZUMAB | PATHWAY | VASCULAR INVASION | ALPHA-3-BETA-1 INTEGRIN | PROTEIN MICROARRAYS | SORAFENIB | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | Humans | Transforming Growth Factor beta1 - metabolism | Vascular Endothelial Growth Factor A - metabolism | Bevacizumab | Antibodies, Monoclonal, Humanized | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Carcinoma, Hepatocellular - blood supply | Liver Neoplasms - pathology | Protein-Serine-Threonine Kinases - metabolism | Pyrazoles - pharmacology | Antibodies, Monoclonal - pharmacology | Angiogenesis Inhibitors - pharmacology | Chick Embryo | Pyrroles - pharmacology | Animals | Receptors, Transforming Growth Factor beta - antagonists & inhibitors | Liver Neoplasms - blood supply | Receptors, Transforming Growth Factor beta - drug effects | Receptors, Transforming Growth Factor beta - metabolism | Carcinoma, Hepatocellular - pathology | Liver Neoplasms - metabolism | Protein-Serine-Threonine Kinases - drug effects | Cell Line, Tumor | Signal Transduction - physiology | Cell Proliferation - drug effects | Neovascularization, Pathologic - metabolism | Embryonic Development - drug effects | Smad Proteins - metabolism | Carcinoma, Hepatocellular - metabolism
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84. Full Text Regulation of Cell Cycle to Stimulate Adult Cardiomyocyte Proliferation and Cardiac Regeneration
by Mohamed, Tamer M.A and Ang, Yen-Sin and Radzinsky, Ethan and Zhou, Ping and Huang, Yu and Elfenbein, Arye and Foley, Amy and Magnitsky, Sergey and Srivastava, Deepak
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
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85. Full Text The transcription factor GLI2 as a downstream mediator of transforming growth factor-β-induced fibroblast activation in SSc
by Liang, Ruifang and Šumová, Barbora and Cordazzo, Cinzia and Mallano, Tatjana and Zhang, Yun and Wohlfahrt, Thomas and Dees, Clara and Ramming, Andreas and Krasowska, Dorota and Michalska-Jakubus, Małgorzata and Distler, Oliver and Schett, Georg and Šenolt, Ladislav and Distler, Jörg H W
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)
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86. Full Text Transforming growth factor β: Tumor suppressor or promoter? Are host immune cells the answer?
by Yang, Li and Moses, Harold L
Cancer Research, ISSN 0008-5472, 11/2008, Volume 68, Issue 22, pp. 9107 - 9111
Therapies targeting transforming growth factor beta (TGF beta) signaling using neutralizing antibodies and small molecular inhibitors are in multiple clinical... 
COLON-CANCER | LUNG METASTASIS | TGF-BETA | EPITHELIA | ANGIOGENESIS | ONCOLOGY | TRANSFORMING-GROWTH-FACTOR-BETA-1 | INFLAMMATION | MICE | PROLIFERATION | MYELOID CELLS | Tumor Suppressor Proteins - physiology | Carcinogens | Animals | Immune System - physiology | Receptors, Chemokine - physiology | Humans | Myeloid Cells - physiology | Transforming Growth Factor beta - physiology | Transforming Growth Factor beta - antagonists & inhibitors | CD11b Antigen - physiology | Signal Transduction - physiology | Inflammation - etiology | Index Medicus
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87. Full Text TGF-β/BMP proteins as therapeutic targets in renal fibrosis. Where have we arrived after 25 years of trials and tribulations?
by Muñoz-Félix, José M and González-Núñez, María and Martínez-Salgado, Carlos and López-Novoa, José M
Pharmacology and Therapeutics, ISSN 0163-7258, 12/2015, Volume 156, pp. 44 - 58
The understanding of renal fibrosis in chronic kidney disease (CKD) remains as a challenge. More than 10% of the population of developed countries suffer from... 
Bone morphogenetic proteins | Smad proteins | TGF-β1 | Inhibitors | Kidney fibrosis | micro-RNAs | EXTRACELLULAR-MATRIX ACCUMULATION | ACTIVATED RECEPTOR-GAMMA | STRUCTURAL-FUNCTIONAL RELATIONSHIPS | TGF-beta 1 | EPITHELIAL-MESENCHYMAL TRANSITION | GROWTH-FACTOR-BETA | KIELIN/CHORDIN-LIKE PROTEIN | TRANSFORMING GROWTH-FACTOR-BETA-1 | INTERSTITIAL FIBROSIS | PPAR-GAMMA | PHARMACOLOGY & PHARMACY | UP-REGULATION | Bone Morphogenetic Proteins - antagonists & inhibitors | Cytokines - metabolism | Kidney - pathology | Signal Transduction | Transforming Growth Factor beta1 - antagonists & inhibitors | Bone Morphogenetic Proteins - agonists | Humans | Transforming Growth Factor beta1 - metabolism | Renal Insufficiency, Chronic - pathology | Bone Morphogenetic Proteins - metabolism | Receptors, Transforming Growth Factor beta - antagonists & inhibitors | Receptors, Transforming Growth Factor beta - metabolism | MicroRNAs | Fibrosis | Smad Proteins - metabolism
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88. Full Text Effects of 4‑Nonylphenol and Bisphenol A on Stimulation of Cell Growth via Disruption of the Transforming Growth Factor‑β Signaling Pathway in Ovarian Cancer Models
by Park, Min-Ah and Choi, Kyung-Chul
Chemical Research in Toxicology, ISSN 0893-228X, 01/2014, Volume 27, Issue 1, pp. 119 - 128
Transforming growth factor β (TGF-β) signaling pathway is a major pathway in cellular processes such as cell growth, apoptosis, and cellular homeostasis. The... 
JUN | CHEMISTRY, MEDICINAL | TGF-BETA | C-FOS | CHEMISTRY, MULTIDISCIPLINARY | BREAST-CANCER | CHEMICALS | ESTROGEN-RECEPTOR-ALPHA | SMAD3 TRANSCRIPTIONAL ACTIVITY | TOXICOLOGY | CYCLE PROGRESSION | SNON | EXPRESSION | Humans | Ovarian Neoplasms - pathology | Benzhydryl Compounds - chemistry | Mice, Knockout | Animals | Signal Transduction - drug effects | Transforming Growth Factor beta - antagonists & inhibitors | Female | Phenols - chemistry | Benzhydryl Compounds - pharmacology | Cell Proliferation - drug effects | Mice | Mice, Inbred BALB C | Ovarian Neoplasms - metabolism | Tumor Cells, Cultured | Transforming Growth Factor beta - metabolism | Disease Models, Animal | Phenols - pharmacology | Index Medicus
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89. Full Text TGF-β signaling in liver and gastrointestinal cancers
by Katz, LH and Likhter, M and Jogunoori, W and Belkin, M and Ohshiro, K and Mishra, L
Cancer Letters, ISSN 0304-3835, 2016, Volume 379, Issue 2, pp. 166 - 172
Highlights • Alteration of TGF-β signaling pathway is associated with liver and gastrointestinal cancers. • The function of TGF-β is context dependent. While... 
Hematology, Oncology and Palliative Medicine | Liver cancer | TGF-β signaling | GI cancers | Cancers | CELL-MEMBRANE | MICROSATELLITE INSTABILITY | KINASE INHIBITOR | TGF-beta signaling | GROWTH-FACTOR-BETA | HEPATOCELLULAR-CARCINOMA | COLORECTAL CARCINOMAS | ONCOLOGY | GASTRIC-CANCER | TUMOR-SUPPRESSOR | MOLECULAR PATHOGENESIS | EXPRESSION | Gastrointestinal Neoplasms - genetics | Liver Neoplasms - genetics | Gastrointestinal Neoplasms - drug therapy | Humans | Gene Expression Regulation, Neoplastic | Liver Neoplasms - drug therapy | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Gastrointestinal Neoplasms - pathology | Animals | Receptors, Transforming Growth Factor beta - antagonists & inhibitors | Transforming Growth Factor beta - genetics | Neoplastic Stem Cells - metabolism | Receptors, Transforming Growth Factor beta - metabolism | Signal Transduction - drug effects | Liver Neoplasms - metabolism | Transforming Growth Factor beta - antagonists & inhibitors | Liver Neoplasms - pathology | Mutation | Transforming Growth Factor beta - metabolism | Gastrointestinal Neoplasms - metabolism | cancers | liver cancer | TGF-β Signaling
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90. Full Text Cutaneous keratoacanthomas/squamous cell carcinomas associated with neutralization of transforming growth factor β by the monoclonal antibody fresolimumab (GC1008)
by Lacouture, Mario E and Morris, John C and Lawrence, Donald P and Tan, Antoinette R and Olencki, Thomas E and Shapiro, Geoffrey I and Dezube, Bruce J and Berzofsky, Jay A and Hsu, Frank J and Guitart, Joan
Cancer Immunology, Immunotherapy, ISSN 0340-7004, 03/2015, Volume 64, Issue 4, pp. 437 - 446
Fresolimumab is an antibody capable of neutralizing all human isoforms of transforming growth factor beta (TGF beta) and has demonstrated anticancer activity... 
GC1008 | Squamous cell cancer | Transforming growth factor β | Fresolimumab | Keratoacanthoma | TGF-BETA | BRAF | IMMUNOLOGY | Transforming growth factor beta | SORAFENIB | MELANOMA | ONCOLOGY | RAS MUTATIONS | SKIN | INHIBITORS | TISSUES | EXPRESSION | MANIFESTATIONS | Transforming Growth Factor beta - immunology | Biomarkers, Tumor - analysis | Skin - metabolism | Carcinoma, Squamous Cell - metabolism | Humans | Antibodies, Monoclonal - adverse effects | Carcinoma, Squamous Cell - chemically induced | Tumor Suppressor Protein p53 - metabolism | Keratoacanthoma - chemically induced | Ki-67 Antigen - metabolism | Skin Neoplasms - chemically induced | Keratoacanthoma - diagnosis | Skin Neoplasms - metabolism | Carcinoma, Squamous Cell - diagnosis | Keratoacanthoma - metabolism | Skin Neoplasms - diagnosis | Transforming Growth Factor beta - antagonists & inhibitors | Skin - drug effects | Skin - immunology
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91. Full Text High-efficiency reprogramming of fibroblasts into cardiomyocytes requires suppression of pro-fibrotic signalling
by Zhao, Yuanbiao and Londono, Pilar and Cao, Yingqiong and Sharpe, Emily J and Proenza, Catherine and O'Rourke, Rebecca and Jones, Kenneth L and Jeong, Mark Y and Walker, Lori A and Buttrick, Peter M and McKinsey, Timothy A and Song, Kunhua
Nature Communications, ISSN 2041-1723, 09/2015, Volume 6, Issue 1, p. 8243
Direct reprogramming of fibroblasts into cardiomyocytes by forced expression of cardiomyogenic factors, GMT (GATA4, Mef2C, Tbx5) or GHMT (GATA4, Hand2, Mef2C,... 
MOUSE FIBROBLASTS | HEART | CARDIAC FIBROBLASTS | CELLS | IN-VITRO | MEF2C | CONVERSION | MULTIDISCIPLINARY SCIENCES | GROWTH | GATA4 | EXPRESSION | Immunohistochemistry | MEF2 Transcription Factors - genetics | Basic Helix-Loop-Helix Transcription Factors - genetics | Cellular Reprogramming Techniques - methods | Myocytes, Cardiac - cytology | Signal Transduction | Embryo, Mammalian | GATA4 Transcription Factor - genetics | T-Box Domain Proteins - genetics | Blotting, Western | rho-Associated Kinases - antagonists & inhibitors | Action Potentials | Animals | Sequence Analysis, RNA | Chromatin Immunoprecipitation | Fibrosis | Myocytes, Cardiac - metabolism | Transforming Growth Factor beta - antagonists & inhibitors | Fibroblasts - cytology | Mice | MicroRNAs - genetics | Cellular Reprogramming - genetics | Real-Time Polymerase Chain Reaction | Fibroblasts - metabolism
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92. Full Text LY2109761, a novel transforming growth factor β receptor type I and type II dual inhibitor, as a therapeutic approach to suppressing pancreatic cancer metastasis
by Davide Melisi and Satoshi Ishiyama and Guido M. Sclabas and Jason B. Fleming and Qianghua Xia and Giampaolo Tortora and James L. Abbruzzese and Paul J. Chiao
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
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93. Full Text The transcription factors snail and slug activate the transforming growth factor-beta signaling pathway in breast cancer
by Dhasarathy, Archana and Phadke, Dhiral and Mav, Deepak and Shah, Ruchir R and Wade, Paul A
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
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