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Arteriosclerosis, thrombosis, and vascular biology, ISSN 1079-5642, 04/2010, Volume 30, Issue 4, pp. 758 - 765
OBJECTIVE—Diet-induced obesity (DIO) in mice causes vascular inflammation and insulin resistance that are accompanied by decreased endothelial-derived NO... 
ENOS | Nitric oxide | Vascular inflammation | nitric oxide | eNOS | ACTIVATED PROTEIN-KINASE | SILDENAFIL | ATHEROSCLEROSIS | ALPHA | ADHESION MOLECULES | ENDOTHELIAL FUNCTION | OVEREXPRESSION | NITRIC-OXIDE PRODUCTION | INHIBITION | vascular inflammation | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | EXPRESSION | Humans | Phosphodiesterase 5 Inhibitors | Male | NF-kappa B - metabolism | Insulin Receptor Substrate Proteins - metabolism | Aortic Diseases - metabolism | Sildenafil Citrate | Inflammation - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Disease Models, Animal | Endothelial Cells - metabolism | Down-Regulation | Enzyme Inhibitors - pharmacology | Aorta, Thoracic - metabolism | Cell Adhesion Molecules - metabolism | Inflammation - etiology | Nitric Oxide Synthase Type III - genetics | Piperazines - pharmacology | Mice, Knockout | Nitric Oxide Synthase Type III - antagonists & inhibitors | Insulin - metabolism | Cyclic GMP - metabolism | Signal Transduction - drug effects | Inflammation - prevention & control | Mice | Endothelial Cells - enzymology | Palmitic Acid - metabolism | Phosphorylation | Phosphatidylinositol 3-Kinases - metabolism | Sulfones - pharmacology | I-kappa B Kinase - metabolism | Dietary Fats | Inflammation Mediators - metabolism | Aorta, Thoracic - drug effects | Nitric Oxide Donors - pharmacology | Nitric Oxide Synthase Type III - metabolism | Cyclic Nucleotide Phosphodiesterases, Type 5 - metabolism | Purines - pharmacology | Mice, Inbred C57BL | Cells, Cultured | Insulin Resistance | Phosphodiesterase Inhibitors - pharmacology | Aorta, Thoracic - physiopathology | Aortic Diseases - physiopathology | Animals | Nitric Oxide - metabolism | Aortic Diseases - etiology | Endothelial Cells - drug effects | Inflammation - physiopathology
Journal Article
Autophagy, ISSN 1554-8635, 2014, Volume 6, Issue 2, pp. 256 - 269
Apoptosis and autophagy have been shown to be negatively regulated by pro-survival Bcl-2 proteins. We determined whether the anti-cancer agent celecoxib, alone... 
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Bcl-2 | ABT-737 | Celecoxib | Autophagy | NSAID | Apoptosis | autophagy | celecoxib | apoptosis | DEATH | ENDOPLASMIC-RETICULUM STRESS | BH3 MIMETIC ABT-737 | CELL BIOLOGY | DRUG-INDUCED APOPTOSIS | SMALL-MOLECULE BCL-2 | PROTEINS | BCL-2 FAMILY-MEMBERS | GROWTH IN-VIVO | CYCLOOXYGENASE-2 INHIBITOR | ENZYME-INHIBITORS
Journal Article
Nature communications, ISSN 2041-1723, 2019, Volume 10, Issue 1, pp. 1897 - 17
The cellular decision regarding whether to undergo proliferation or death is made at the restriction (R)-point, which is disrupted in nearly all tumors. The... 
UBIQUITINATION | AML1-ETO | ACETYLATION | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | PROTEINS | QUANTITATIVE-ANALYSIS | POLYCOMB | CANCER | KINASES | FAMILY | Chromatin - metabolism | RNA, Small Interfering - genetics | Myeloid-Lymphoid Leukemia Protein - metabolism | TOR Serine-Threonine Kinases - metabolism | Core Binding Factor Alpha 3 Subunit - antagonists & inhibitors | Humans | Polycomb-Group Proteins - metabolism | TOR Serine-Threonine Kinases - genetics | Cell Cycle Checkpoints - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Chromatin - chemistry | MAP Kinase Kinase 1 - antagonists & inhibitors | Butadienes - pharmacology | Signal Transduction | Epithelial Cells - pathology | MAP Kinase Kinase 1 - metabolism | Imidazoles - pharmacology | Cyclin-Dependent Kinase 4 - metabolism | Piperazines - pharmacology | Cell Cycle Checkpoints - drug effects | Polycomb-Group Proteins - genetics | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Line, Tumor | MAP Kinase Kinase 4 - genetics | RNA, Small Interfering - metabolism | ras Proteins - genetics | Core Binding Factor Alpha 3 Subunit - metabolism | Epithelial Cells - metabolism | Nitriles - pharmacology | Cyclin-Dependent Kinase 4 - genetics | Epithelial Cells - drug effects | ras Proteins - metabolism | Drosophila melanogaster - genetics | Chromatin Assembly and Disassembly - drug effects | Drosophila melanogaster - metabolism | MAP Kinase Kinase 1 - genetics | TOR Serine-Threonine Kinases - antagonists & inhibitors | MAP Kinase Kinase 4 - metabolism | HEK293 Cells | MAP Kinase Kinase 4 - antagonists & inhibitors | Chromatin - drug effects | Histone-Lysine N-Methyltransferase - genetics | Drosophila melanogaster - cytology | Gene Expression Regulation | p38 Mitogen-Activated Protein Kinases - genetics | Sirolimus - pharmacology | Animals | Histone-Lysine N-Methyltransferase - metabolism | Myeloid-Lymphoid Leukemia Protein - genetics | Core Binding Factor Alpha 3 Subunit - genetics | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Polycomb group proteins | Regulators | Molecular modelling | S phase | Genes | Cell cycle | Loci | Runx3 protein | Recruitment | Tumors | Chromatin remodeling
Journal Article
Oncogene, ISSN 0950-9232, 10/2011, Volume 30, Issue 41, pp. 4261 - 4274
In the presence of sustained DNA damage occurring in S-phase or G2, normal cells arrest before mitosis and eventually become senescent. The checkpoint kinases... 
cyclin B1 | ATM | Chk2 | G2-M checkpoint | cell cycle | GENOTOXIC STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOTIC CATASTROPHE | TRANSCRIPTIONAL REPRESSION | G CHECKPOINT | CELL BIOLOGY | GENOMIC INSTABILITY | RETINOBLASTOMA PROTEIN | ONCOLOGY | GENETICS & HEREDITY | P53-DEFICIENT CELLS | CELL-CYCLE EXIT | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | Protein Kinases - metabolism | G2 Phase Cell Cycle Checkpoints - physiology | Phosphorylation | Protein Kinases - genetics | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Immunoblotting | Male | Cyclin B1 - metabolism | Pyrones - pharmacology | Tumor Suppressor Protein p53 - genetics | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | RNA Interference | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Antineoplastic Agents - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | HCT116 Cells | Cell Cycle Proteins - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin B1 - genetics | Morpholines - pharmacology | Signal Transduction - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Piperazines - pharmacology | G2 Phase Cell Cycle Checkpoints - genetics | Signal Transduction - drug effects | Cell Line, Tumor | Checkpoint Kinase 2 | Bleomycin - pharmacology | Checkpoint Kinase 1 | Signal Transduction - physiology | DNA Damage | HeLa Cells | Cell division | Oxidative stress | Signal transduction | DNA damage | Cyclin-dependent kinases | Cell cycle | CHK2 protein | Epithelial cells | Mitosis | CHK1 protein | G2 phase | Genotoxicity | Osteosarcoma cells | p53 protein | Cyclin-dependent kinase | Chemotherapy | Fibroblasts | Cancer | Life Sciences | Biochemistry, Molecular Biology
Journal Article
Cancer cell, ISSN 1535-6108, 2006, Volume 10, Issue 5, pp. 375 - 388
BCL-2 proteins are critical for cell survival and are overexpressed in many tumors. ABT-737 is a small-molecule BH3 mimetic that exhibits single-agent activity... 
CELLCYCLE | PROGRAMMED CELL-DEATH | CANCER-CELLS | STEM-CELLS | PROAPOPTOTIC ACTIVITY | ONCOLOGY | X-L | ACUTE MYELOGENOUS LEUKEMIA | IN-VIVO | MITOCHONDRIAL-MEMBRANE | BCL-2 FAMILY-MEMBERS | BH3-ONLY PROTEINS | RNA, Small Interfering - genetics | bcl-2-Associated X Protein - chemistry | Humans | Leukemia, Myeloid, Acute - metabolism | Nitrophenols - metabolism | bcl-2 Homologous Antagonist-Killer Protein - genetics | Piperazines - metabolism | Neoplasm Proteins - metabolism | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Biphenyl Compounds - metabolism | Biphenyl Compounds - therapeutic use | Recombinant Fusion Proteins - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Nitrophenols - therapeutic use | Hematopoietic Stem Cells - physiology | Leukemia, Myeloid, Acute - drug therapy | Proto-Oncogene Proteins c-bcl-2 - chemistry | Dimerization | bcl-2-Associated X Protein - genetics | Protein Structure, Tertiary | Cell Line | bcl-2-Associated X Protein - metabolism | Piperazines - therapeutic use | Animals | Sulfonamides - therapeutic use | Myeloid Cell Leukemia Sequence 1 Protein | Sulfonamides - metabolism | Recombinant Fusion Proteins - genetics | Protein Conformation | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | Mice | Apoptosis - physiology | Drug Resistance, Neoplasm - physiology | Proto-Oncogene Proteins c-bcl-2 - genetics | RNA, Small Interfering - metabolism | Proteins | Oncology, Experimental | Lung cancer | Bone marrow | Transplantation | Lymphomas | Research | Hematopoietic stem cells | Cancer | Apoptosis
Journal Article
Circulation (New York, N.Y.), ISSN 0009-7322, 12/2010, Volume 122, Issue 24, pp. 2619 - 2633
proton pump inhibitors | antiplatelet drugs | gastrointestinal hemorrhage | platelet aggregation inhibitors | aspirin | thienopyridine | AHA Scientific Statements | CYTOCHROME-P450 | CARDIAC & CARDIOVASCULAR SYSTEMS | MYOCARDIAL-INFARCTION | ACID SUPPRESSION | PERCUTANEOUS CORONARY INTERVENTION | CLOPIDOGREL | LOW-DOSE ASPIRIN | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | DISEASE | PERIPHERAL VASCULAR DISEASE | PRASUGREL | PEPTIC-ULCERS | Piperazines - administration & dosage | Prasugrel Hydrochloride | Purinergic P2Y Receptor Antagonists - administration & dosage | Thiophenes - adverse effects | Cardiovascular Diseases - drug therapy | Humans | Thienopyridines - adverse effects | Thienopyridines - metabolism | Piperazines - metabolism | Thiophenes - metabolism | Thiophenes - administration & dosage | Aspirin - administration & dosage | Purinergic P2Y Receptor Antagonists - metabolism | Histamine H2 Antagonists - administration & dosage | Purinergic P2Y Receptor Antagonists - adverse effects | Drug Interactions | Proton Pump Inhibitors - administration & dosage | Aspirin - adverse effects | Aspirin - metabolism | Platelet Aggregation Inhibitors - administration & dosage | Ticlopidine - adverse effects | Ticlopidine - metabolism | Ticlopidine - administration & dosage | Anti-Inflammatory Agents, Non-Steroidal - metabolism | Platelet Aggregation Inhibitors - metabolism | Drug Therapy, Combination | Platelet Aggregation Inhibitors - adverse effects | Proton Pump Inhibitors - adverse effects | Thienopyridines - administration & dosage | Risk Factors | Histamine H2 Antagonists - adverse effects | Piperazines - adverse effects | Ticlopidine - analogs & derivatives | Aryl Hydrocarbon Hydroxylases - metabolism | Gastrointestinal Hemorrhage - chemically induced | Gastrointestinal Hemorrhage - prevention & control | Histamine H2 Antagonists - metabolism | Anti-Inflammatory Agents, Non-Steroidal - adverse effects | Cytochrome P-450 CYP2C19 | Anti-Inflammatory Agents, Non-Steroidal - administration & dosage | Proton Pump Inhibitors - metabolism
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 06/2006, Volume 116, Issue 6, pp. 1561 - 1570
Metastasis is the major cause of cancer morbidity, but strategies for direct interference with invasion processes are lacking. Dedifferentiated, late-stage... 
BREAST-CANCER | MEDICINE, RESEARCH & EXPERIMENTAL | FACTOR-BETA | 3D CULTURES | GROWTH-FACTOR-RECEPTOR | TRANSFORMED PHENOTYPE | EPITHELIAL-MESENCHYMAL TRANSITIONS | CELL-LINES | NF-KAPPA-B | MOLECULAR-MECHANISMS | INCREASED MALIGNANCY | Humans | ras Proteins - metabolism | Mammary Tumor Virus, Mouse - metabolism | Piperazines - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Mammary Neoplasms, Experimental - metabolism | Recombinant Fusion Proteins - metabolism | Pyrimidines - metabolism | Breast Neoplasms - metabolism | Antineoplastic Agents - metabolism | Epithelial Cells - physiology | Neoplasm Metastasis | Mammary Neoplasms, Experimental - pathology | Female | Epithelial Cells - cytology | Cell Differentiation - physiology | Receptor, Platelet-Derived Growth Factor beta - metabolism | Autocrine Communication | Receptor, Platelet-Derived Growth Factor alpha - metabolism | Mice, Transgenic | Imatinib Mesylate | Animals | Transforming Growth Factor beta - genetics | Breast Neoplasms - pathology | Mice, Nude | Cell Line, Tumor | Mesoderm - physiology | Recombinant Fusion Proteins - genetics | Signal Transduction - physiology | Mice | Benzamides | Enzyme Activation | Mammary Tumor Virus, Mouse - genetics | Transforming Growth Factor beta - metabolism | Apoptosis | Protein Kinase Inhibitors - metabolism | Medicine, Experimental | Medical research | Breast cancer | Research | Metastasis | Drug therapy
Journal Article
Journal Article
Molecular biology of the cell, ISSN 1059-1524, 05/2006, Volume 17, Issue 5, pp. 2287 - 2302
Cohesin maintains sister chromatid cohesion until its Rad21/Scc1/Mcd1 is cleaved by separase during anaphase. DNA topoisomerase II (topo II) maintains the... 
SISTER-CHROMATID COHESION | XENOPUS EGG EXTRACTS | FISSION YEAST | ASSEMBLY CHECKPOINT | LIVING MAMMALIAN-CELLS | MITOTIC CHROMOSOMES | DNA TOPOISOMERASE-II | DE-LANGE-SYNDROME | SACCHAROMYCES-CEREVISIAE | VERTEBRATE COHESIN | CELL BIOLOGY | Protein Kinases - metabolism | Chromatin - metabolism | Cell Cycle Proteins - analysis | Protein Kinases - genetics | Humans | Protein-Serine-Threonine Kinases | Centromere - metabolism | Mitosis - genetics | Phosphoproteins - metabolism | Repressor Proteins - analysis | Cyclin B1 | Cell Nucleus - metabolism | Spindle Apparatus - metabolism | RNA Interference | Topoisomerase II Inhibitors | Cell Cycle Proteins - genetics | Mad2 Proteins | Telomere - metabolism | Nuclear Proteins - genetics | Kinetochores - chemistry | Repressor Proteins - metabolism | Calcium-Binding Proteins - metabolism | DNA Topoisomerases, Type II - metabolism | Repetitive Sequences, Nucleic Acid - genetics | Protein Kinases - analysis | Chromosomal Proteins, Non-Histone - metabolism | Kinetochores - metabolism | Calcium-Binding Proteins - analysis | Cell Cycle Proteins - metabolism | Enzyme Inhibitors - pharmacology | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Chromosomes, Human - metabolism | Phosphoproteins - genetics | Piperazines - pharmacology | Proteins - genetics | Proteins - metabolism | Metaphase - genetics | Cyclin B - metabolism | DNA Topoisomerases, Type II - genetics | HeLa Cells | Calcium-Binding Proteins - genetics
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 0027-8424, 6/2011, Volume 108, Issue 24, pp. 9951 - 9956
The tyrosine kinase c-Met promotes the formation and malignant progression of multiple cancers. It is well known that c-Met hyperactivation increases... 
Phenotypes | Cell growth | Hepatocytes | Somatic cells | Induced pluripotent stem cells | Neurons | Stem cells | Glioblastoma | Neural stem cells | Tumors | Cancer stem cell | Oct4 | Sox2 | Klf4 | Hepatocyte growth factor | CANCER-CELLS | MULTIDISCIPLINARY SCIENCES | FACTOR EXPRESSION | PROLIFERATION | TUMORIGENICITY | TUMOR-INITIATING CELLS | P53 | cancer stem cell | PATHWAY | hepatocyte growth factor | IN-VIVO | GROWTH-FACTOR | DIFFERENTIATION | Proto-Oncogene Proteins c-met - metabolism | Homeodomain Proteins - metabolism | Humans | Glycoproteins - metabolism | Peptides - genetics | Immunoblotting | Transplantation, Heterologous | Antigens, CD - genetics | Antigens, CD - metabolism | Cellular Reprogramming | SOXB1 Transcription Factors - metabolism | Neoplasms, Experimental - pathology | Octamer Transcription Factor-3 - genetics | Flow Cytometry | Peptides - metabolism | Glioblastoma - genetics | Neoplastic Stem Cells - metabolism | RNA Interference | SOXB1 Transcription Factors - genetics | Neoplasms, Experimental - genetics | Neoplastic Stem Cells - pathology | Glioblastoma - metabolism | Indoles - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Tumor Cells, Cultured | Glycoproteins - genetics | Nanog Homeobox Protein | Signal Transduction | Proto-Oncogene Proteins c-met - antagonists & inhibitors | Mice, SCID | Reverse Transcriptase Polymerase Chain Reaction | Sulfonamides - pharmacology | AC133 Antigen | Piperazines - pharmacology | Proto-Oncogene Proteins c-myc - metabolism | Homeodomain Proteins - genetics | Proto-Oncogene Proteins c-met - genetics | Phenotype | Animals | Glioblastoma - pathology | Octamer Transcription Factor-3 - metabolism | Mice | Proto-Oncogene Proteins c-myc - genetics | Neoplasms, Experimental - metabolism | Physiological aspects | Development and progression | Cellular signal transduction | Genetic aspects | Research | Glioblastoma multiforme | Protein kinases | Biological Sciences
Journal Article
The American journal of gastroenterology, ISSN 0002-9270, 12/2010, Volume 105, Issue 12, pp. 2533 - 2549
This expert consensus document was developed by the American College of Cardiology Foundation (ACCF), the American College of Gastroenterology (ACG), and the... 
proton pump inhibitors | aspirin | ACCF Expert Consensus Document antiplatelet drugs | gastrointestinal hemorrhage | thienopyridine | platelet aggregation inhibitors | CYTOCHROME-P450 | MYOCARDIAL-INFARCTION | ACID SUPPRESSION | PERCUTANEOUS CORONARY INTERVENTION | CLOPIDOGREL | LOW-DOSE ASPIRIN | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | DISEASE | PRASUGREL | GASTROENTEROLOGY & HEPATOLOGY | PEPTIC-ULCERS | Piperazines - administration & dosage | Prasugrel Hydrochloride | Purinergic P2Y Receptor Antagonists - administration & dosage | Thiophenes - adverse effects | Cardiovascular Diseases - drug therapy | Humans | Thienopyridines - adverse effects | Thienopyridines - metabolism | Piperazines - metabolism | Thiophenes - metabolism | Thiophenes - administration & dosage | Aspirin - administration & dosage | Purinergic P2Y Receptor Antagonists - metabolism | Histamine H2 Antagonists - administration & dosage | Purinergic P2Y Receptor Antagonists - adverse effects | Drug Interactions | Proton Pump Inhibitors - administration & dosage | Aspirin - adverse effects | Aspirin - metabolism | Platelet Aggregation Inhibitors - administration & dosage | Ticlopidine - adverse effects | Ticlopidine - metabolism | Ticlopidine - administration & dosage | Anti-Inflammatory Agents, Non-Steroidal - metabolism | Platelet Aggregation Inhibitors - metabolism | Drug Therapy, Combination | Platelet Aggregation Inhibitors - adverse effects | Proton Pump Inhibitors - adverse effects | Thienopyridines - administration & dosage | Risk Factors | Histamine H2 Antagonists - adverse effects | Piperazines - adverse effects | Ticlopidine - analogs & derivatives | Aryl Hydrocarbon Hydroxylases - metabolism | Gastrointestinal Hemorrhage - chemically induced | Gastrointestinal Hemorrhage - prevention & control | Histamine H2 Antagonists - metabolism | Anti-Inflammatory Agents, Non-Steroidal - adverse effects | Cytochrome P-450 CYP2C19 | Anti-Inflammatory Agents, Non-Steroidal - administration & dosage | Proton Pump Inhibitors - metabolism
Journal Article
British journal of cancer, ISSN 1532-1827, 2008, Volume 99, Issue 4, pp. 622 - 631
Little is known about the factors that enable the mobilisation of human mesenchymal stem cells (MSC) from the bone marrow into the blood stream and their... 
Angiogenesis | MSC | Pancreas | Lentivirus | VEGF | angiogenesis | PHENOTYPE | HYPOXIA | DELIVERY | ADHESION | VEHICLES | ONCOLOGY | pancreas | GENERATION | DIFFERENTIATION | TUMOR STROMA | MARROW STROMAL CELLS | lentivirus | ENDOTHELIAL GROWTH-FACTOR | Endothelium, Vascular - cytology | Cell Proliferation | Pancreatic Neoplasms - metabolism | Humans | Pancreatic Neoplasms - blood supply | Actins - metabolism | Spheroids, Cellular - pathology | Endothelium, Vascular - drug effects | Male | Transplantation, Heterologous | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - antagonists & inhibitors | Bevacizumab | Antibodies, Monoclonal, Humanized | Muscle, Smooth - drug effects | Umbilical Veins - drug effects | Lentivirus - genetics | Antineoplastic Agents - pharmacology | Cetuximab | Umbilical Veins - cytology | Fibroblasts - metabolism | Antibodies, Monoclonal - pharmacology | Pancreatic Neoplasms - pathology | Cells, Cultured | Angiogenesis Inhibitors - pharmacology | Mesenchymal Stromal Cells - metabolism | Epidermal Growth Factor - metabolism | Muscle, Smooth - metabolism | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Cell Movement - drug effects | Platelet-Derived Growth Factor - metabolism | Animals | Cell Differentiation - drug effects | Endothelium, Vascular - metabolism | Mice, Nude | Fibroblasts - drug effects | Epidermal Growth Factor - antagonists & inhibitors | Fibroblasts - cytology | Mice | Neovascularization, Pathologic - metabolism | Benzamides | Muscle, Smooth - cytology | Platelet-Derived Growth Factor - antagonists & inhibitors | Mesenchymal Stem Cell Transplantation | Umbilical Veins - metabolism | Translational Therapeutics
Journal Article