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Journal Article
Blood, ISSN 0006-4971, 08/2008, Volume 112, Issue 4, pp. 1503 - 1509
Journal Article
Journal Article
Nature, ISSN 0028-0836, 02/2011, Volume 470, Issue 7333, pp. 269 - 276
Journal Article
Circulation Research, ISSN 0009-7330, 02/2016, Volume 118, Issue 3, pp. 388 - 399
RATIONALE:Aortic aneurysm is a life-threatening cardiovascular disorder caused by the predisposition for dissection and rupture. Genetic studies have proved... 
Smooth muscle | Myocytes | Macrophages | Aortic aneurysm | Aortic rupture | Smad4 protein | myocytes, smooth muscle | CARDIAC & CARDIOVASCULAR SYSTEMS | HEREDITARY HEMORRHAGIC TELANGIECTASIA | ENDOTHELIAL SMAD4 | ATHEROSCLEROSIS | RECEPTOR | JUVENILE POLYPOSIS SYNDROME | aortic aneurysm | macrophages | GROWTH-FACTOR-BETA | aortic rupture | PERIPHERAL VASCULAR DISEASE | MUTATIONS | METALLOELASTASE | HEMATOLOGY | EXPRESSION | CONTRIBUTES | Protein-Serine-Threonine Kinases - deficiency | Up-Regulation | Receptors, Transforming Growth Factor beta - genetics | Aortic Aneurysm - metabolism | Muscle, Smooth, Vascular - metabolism | Myocytes, Smooth Muscle - pathology | Male | Aorta - metabolism | Transfection | RNA Interference | Smad4 Protein - genetics | Time Factors | Proteolysis | Female | Aortic Aneurysm - pathology | Myocytes, Smooth Muscle - metabolism | Aortic Aneurysm - prevention & control | Cell Line | Elastin - metabolism | Genetic Predisposition to Disease | Mice, Inbred C57BL | Protein-Serine-Threonine Kinases - genetics | Rats | Matrix Metalloproteinase 12 - metabolism | Chemotaxis | Smad4 Protein - metabolism | Mice, Knockout | Aorta - pathology | Macrophages - metabolism | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Cathepsins - metabolism | Chemokines - metabolism | Smad4 Protein - deficiency | Aortic Aneurysm - genetics | Receptors, Transforming Growth Factor beta - deficiency
Journal Article
Molecular Medicine Reports, ISSN 1791-2997, 7/2015, Volume 12, Issue 1, pp. 192 - 198
Doxorubicin (Dox) is a commonly used chemotherapeutic drug in human colon cancer. However, it becomes increasingly ineffective with tumor progression, the... 
doxorubicin chemoresistance | epithelial-mesenchymal transition | transforming growth factor β/Smad4 signaling | RNA interference | colon cancer | Epithelial-mesenchymal transition | Transforming growth factor β/Smad4 signaling | Colon cancer | Doxorubicin chemoresistance | RNA, Small Interfering - genetics | Smad4 Protein - antagonists & inhibitors | Antibiotics, Antineoplastic - pharmacology | Cadherins - metabolism | Signal Transduction | Vimentin - metabolism | HCT116 Cells | Humans | Gene Expression Regulation, Neoplastic | Epithelial-Mesenchymal Transition - drug effects | Transcription Factors - genetics | Epithelial-Mesenchymal Transition - genetics | Smad4 Protein - metabolism | Transcription Factors - metabolism | Drug Resistance, Neoplasm - genetics | Transforming Growth Factor beta - genetics | Smad4 Protein - genetics | Vimentin - genetics | Cadherins - genetics | Snail Family Transcription Factors | Transforming Growth Factor beta - metabolism | Doxorubicin - pharmacology | Drug Resistance, Neoplasm - drug effects | RNA, Small Interfering - metabolism | Biotechnology | Immunoglobulins | Phosphorylation | Substance abuse treatment | Transcription factors | Mesenchyme | Transforming growth factor | RNA-mediated interference | Multidrug resistance | Colorectal cancer | Chemoresistance | Drug resistance | Kinases | Gene expression | Doxorubicin | Smad4 protein | Studies | Chemotherapy | Rodents | Colon | Growth factors | Apoptosis | Smad4 signaling | transforming growth factor β
Journal Article
Journal Article
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 05/2015, Volume 308, Issue 10, pp. F1167 - F1177
Diabetic nephropathy is characterized by diffuse mesangial matrix expansion and is largely dependent on the TGF-beta/Smad signaling pathway. Smad4 is required... 
Diabetic nephropathy | AICAR | Smad4 | AMP-activated protein kinase | High glucose | PHYSIOLOGY | TGF-BETA | TUMOR-SUPPRESSOR SMAD4 | RENAL HYPERTROPHY | GROWTH-FACTOR-BETA | high glucose | INFLAMMATION | IN-VIVO | DISEASE | GENE-EXPRESSION | UROLOGY & NEPHROLOGY | TRANSCRIPTION FACTOR | diabetic nephropathy | AMP-Activated Protein Kinases - metabolism | Smad4 Protein - antagonists & inhibitors | Male | AMP-Activated Protein Kinases - drug effects | Aminoimidazole Carboxamide - pharmacology | Mesangial Cells - drug effects | Ribonucleotides - pharmacology | Smad4 Protein - drug effects | Cell Nucleus - metabolism | Diabetes Mellitus, Experimental - chemically induced | Diabetes Mellitus, Experimental - complications | Streptozocin - adverse effects | Disease Models, Animal | Cell Line | Diabetic Nephropathies - pathology | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Glucose - pharmacology | Mesangial Cells - metabolism | Smad4 Protein - metabolism | Hypoglycemic Agents - pharmacology | Transforming Growth Factor beta - pharmacology | Animals | Aminoimidazole Carboxamide - analogs & derivatives | Mesangial Cells - pathology | Signal Transduction - physiology | Biological Transport - physiology | Mice | In Vitro Techniques | Transforming Growth Factor beta - metabolism | Transcription factors | Biological transport | Diabetic nephropathies | Development and progression | Genetic aspects | Properties | Protein kinases
Journal Article
Oncotarget, ISSN 1949-2553, 2016, Volume 7, Issue 29, pp. 45199 - 45213
Journal Article
Gastroenterology, ISSN 0016-5085, 2012, Volume 142, Issue 3, pp. 562 - 571.e2
Journal Article
Cancer Research, ISSN 0008-5472, 02/2011, Volume 71, Issue 3, pp. 998 - 1008
Journal Article