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STEM CELLS, ISSN 1066-5099, 03/2010, Volume 28, Issue 3, pp. 564 - 572
Human mesenchymal stem cells (hMSCs) are multipotent cells that can differentiate into many cell types. Chondrogenesis is induced in hMSCs cultured as a... 
N‐cadherin | Cell shape | Rac1 | Chondrogenesis | Smooth muscle cells | Mesenchymal stem cells | N-cadherin | MYOBLAST FUSION | CELL & TISSUE ENGINEERING | CELL BIOLOGY | ADHESION | ONCOLOGY | MESENCHYMAL PROGENITOR CELLS | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | GENE-EXPRESSION | CYTOSKELETAL TENSION | DIFFERENTIATION | RHO-GTPASES | PROTEINS | HEMATOLOGY | MODULATION | MAMMARY EPITHELIAL-CELLS | Chondrocytes - cytology | Chondrogenesis - drug effects | Cadherins - metabolism | Humans | Extracellular Matrix - metabolism | Antigens, CD - genetics | Cell Lineage - drug effects | Transforming Growth Factor beta3 - metabolism | Antigens, CD - metabolism | Cell Differentiation - genetics | Chondrocytes - drug effects | Mesenchymal Stromal Cells - cytology | Cadherins - genetics | Myocytes, Smooth Muscle - drug effects | Myocytes, Smooth Muscle - cytology | Myocytes, Smooth Muscle - metabolism | Chondrocytes - metabolism | Transforming Growth Factor beta3 - pharmacology | Mesenchymal Stromal Cells - drug effects | Cell Adhesion - genetics | Muscle Development - physiology | Cells, Cultured | Gene Expression Regulation - physiology | Mesenchymal Stromal Cells - metabolism | Up-Regulation - genetics | Antigens, CD - drug effects | Cadherins - drug effects | Cell Adhesion - drug effects | Cell Lineage - physiology | Cell Shape - drug effects | Gene Expression Regulation - drug effects | Up-Regulation - drug effects | Chondrogenesis - physiology | Muscle Development - drug effects | rac1 GTP-Binding Protein - drug effects | Cell Differentiation - drug effects | Cell Shape - physiology | rac1 GTP-Binding Protein - metabolism | rac1 GTP-Binding Protein - genetics
Journal Article
Nature Communications, ISSN 2041-1723, 2012, Volume 3, Issue 1, p. 1208
Journal Article
American Journal of Pathology, The, ISSN 0002-9440, 2012, Volume 181, Issue 6, pp. 2188 - 2201
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 05/2005, Volume 203, Issue 2, pp. 398 - 409
Human mesenchymal stem cells (hMSCs) expanded with and without fibroblast growth factor (FGF) supplementation were compared with respect to their proliferation... 
PROGENITOR CELLS | CROSS-TALK | PROTEIN-KINASE-C | IN-VITRO | PHYSIOLOGY | ATDC5 CELLS | DEFICIENT MDX MICE | STROMAL CELLS | GENE-EXPRESSION SIGNATURES | CHONDROCYTE DIFFERENTIATION | N-CADHERIN | CELL BIOLOGY | Chondrocytes - cytology | Chondrogenesis - drug effects | Age Factors | Oligonucleotide Array Sequence Analysis | Humans | Fibroblast Growth Factor 2 - pharmacology | Bone Marrow Cells - physiology | Gene Expression Profiling | Cell Culture Techniques - methods | Proteoglycans - drug effects | Cell Differentiation - genetics | Chondrocytes - drug effects | Mesenchymal Stromal Cells - cytology | Chondrocytes - physiology | Collagen - drug effects | Up-Regulation - physiology | Bone Marrow Cells - drug effects | Mesenchymal Stromal Cells - physiology | Mesenchymal Stromal Cells - drug effects | Tissue Engineering - methods | Bone Marrow Cells - cytology | Gene Expression Regulation - genetics | Extracellular Matrix Proteins - genetics | Cells, Cultured | Proteoglycans - metabolism | Down-Regulation - drug effects | Extracellular Matrix Proteins - drug effects | Down-Regulation - physiology | Gene Expression Regulation - drug effects | Up-Regulation - drug effects | Chondrogenesis - physiology | Collagen - metabolism | Mitosis - drug effects | Mitosis - physiology | Signal Transduction - drug effects | Cell Differentiation - drug effects | Signal Transduction - physiology | Cell Proliferation - drug effects
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 8, p. e24099
Background: MicroRNA-34a (miR-34a) is a transcriptional target of p53 and is down-regulated in pancreatic cancer. This study aimed to investigate the... 
BIOMARKERS | NERVOUS-SYSTEM | APOPTOSIS | TRAIL | P53 PROTEIN | MULTIDISCIPLINARY SCIENCES | TUMOR-SUPPRESSOR | NOTCH SIGNALING PATHWAY | MICRORNAS | EXPRESSION | TUMORIGENESIS | Cell Cycle - genetics | Chromatin - metabolism | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Humans | Spheroids, Cellular - pathology | Apoptosis - genetics | Epithelial-Mesenchymal Transition - drug effects | MicroRNAs - metabolism | Epithelial-Mesenchymal Transition - genetics | Pancreatic Neoplasms - drug therapy | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - pathology | Epigenesis, Genetic - drug effects | Spheroids, Cellular - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Hydroxamic Acids - pharmacology | Tumor Stem Cell Assay | Neoplasm Invasiveness | Pancreatic Neoplasms - pathology | Spheroids, Cellular - metabolism | Pancreatic Neoplasms - genetics | Up-Regulation - genetics | Up-Regulation - drug effects | Azacitidine - pharmacology | Cell Movement - drug effects | Cell Line, Tumor | Hydroxamic Acids - therapeutic use | Cell Proliferation - drug effects | MicroRNAs - genetics | Cell Cycle - drug effects | Azacitidine - therapeutic use | Prevention | Epigenetic inheritance | Care and treatment | Chemotherapy | Chromatin | Pancreatic cancer | Stem cells | Development and progression | Tumor proteins | Cancer | Apoptosis | Bcl-2 protein | p53 Protein | Metastasis | Caspase-3 | Cancer therapies | Toxicology | Scholarships & fellowships | Cell growth | N-Cadherin | Restoration | Physiology | Tumorigenesis | Inhibition | MiRNA | Gene expression | SIRT1 protein | Pathology | Biomarkers | Notch protein | Mutation | Cell proliferation | Azacytidine | Histone deacetylase | Transcription | Mesenchyme | Laboratories | Leukemia | Gene regulation | Multiple myeloma | E-cadherin | Modulators | Cell cycle | Inducers | Departments | Caspase | Pharmacology | Breast cancer | Tumor cell lines | Ribonucleic acid--RNA | Medicine | Cyclin-dependent kinase inhibitor p21 | Medical prognosis | Reagents | Cell lines | Epigenetics | Cyclin-dependent kinase inhibitor p27 | Prostate cancer | RNA | Ribonucleic acid
Journal Article
PLoS ONE, ISSN 1932-6203, 01/2015, Volume 10, Issue 1, p. e0116747
Cellular mechanisms of multidrug resistance (MDR) are related to ABC transporters, apoptosis, antioxidation, drug metabolism, DNA repair and cell... 
EPITHELIAL-MESENCHYMAL TRANSITION | BREAST-CANCER CELLS | STEM-CELLS | MDR1 | TRANSPORTERS | MULTIDISCIPLINARY SCIENCES | DOWN-REGULATION | MUTANT P53 | TUMOR-SUPPRESSOR PROTEIN | DRUG-RESISTANCE | OVARIAN-CANCER | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Drug Resistance, Multiple - drug effects | Genes, Neoplasm | Humans | Apoptosis - genetics | Epithelial-Mesenchymal Transition - drug effects | Gene Expression Profiling | DNA Repair - genetics | Epithelial-Mesenchymal Transition - genetics | Neoplasm Proteins - metabolism | Dose-Response Relationship, Drug | MCF-7 Cells | Neoplastic Stem Cells - metabolism | Inhibitory Concentration 50 | Gene Expression Regulation, Neoplastic - drug effects | Neoplasm Proteins - genetics | DNA Repair - drug effects | Drug Resistance, Multiple - genetics | Tumor Suppressor Protein p53 - metabolism | Signal Transduction - genetics | Down-Regulation - drug effects | Cell Shape - drug effects | Up-Regulation - drug effects | Drug Resistance, Neoplasm - genetics | Breast Neoplasms - genetics | Signal Transduction - drug effects | Doxorubicin - pharmacology | Drug Resistance, Neoplasm - drug effects | Physiological aspects | Drug resistance in microorganisms | Anthracyclines | Tumor proteins | Intermediate filament proteins | Genes | Bcl-2 protein | AKT protein | Cytotoxicity | Drug resistance | Cancer therapies | Doxorubicin | Cell morphology | Proteins | CD44 antigen | Drug metabolism | Repair | Drug dosages | Deoxyribonucleic acid--DNA | Enzymes | Ploidy | BRCA1 protein | Gene expression | Metabolism | 1-Phosphatidylinositol 3-kinase | Chemotherapy | Pharmacy | Stem cells | Mutation | Codons | Surface markers | Cell proliferation | Transcription | Mesenchyme | Gene regulation | Cytology | Kinases | DNA repair | Cell surface | E-cadherin | MDR1 protein | Clonal deletion | Rodents | Cell cycle | Deletion | Pharmaceutical sciences | Glutathione | Multidrug resistance | Breast cancer | Medicine | Hypotheses | Gene amplification | Apoptosis | Tumors | Deoxyribonucleic acid | DNA
Journal Article
Development (Cambridge), ISSN 0950-1991, 11/2013, Volume 140, Issue 22, pp. 4510 - 4521
Muller glia function as retinal stem cells in adult zebrafish. In response to loss of retinal neurons, Muller glia partially dedifferentiate, re-express... 
Müller glia | N-cadherin | Retinal regeneration | Alcama | Muller glia | STEM-CELLS | DEDIFFERENTIATION | PROLIFERATION | DEVELOPMENTAL BIOLOGY | GOLDFISH RETINA | ADULT ZEBRAFISH | VERTEBRATE RETINA | ROD PHOTORECEPTORS | SIGNALING PATHWAY | NEUROGENESIS | LINEAGE | Cadherins - metabolism | Multipotent Stem Cells - metabolism | Photoreceptor Cells, Vertebrate - drug effects | Ependymoglial Cells - metabolism | Neural Stem Cells - cytology | Neuroepithelial Cells - cytology | Retinal Ganglion Cells - metabolism | Retinal Neurons - cytology | Retinal Ganglion Cells - cytology | Neurogenesis - drug effects | Retinal Neurons - drug effects | Asymmetric Cell Division - drug effects | Ouabain - pharmacology | Biomarkers - metabolism | Cell Dedifferentiation - drug effects | Zebrafish Proteins - metabolism | Neural Stem Cells - drug effects | Photoreceptor Cells, Vertebrate - cytology | Cell Adhesion - drug effects | Ependymoglial Cells - drug effects | Regeneration - drug effects | Animals | Retinal Neurons - metabolism | Models, Biological | Multipotent Stem Cells - cytology | Zebrafish - metabolism | Ependymoglial Cells - cytology | Heterozygote | Neuroepithelial Cells - metabolism | Photoreceptor Cells, Vertebrate - metabolism | Cell Cycle - drug effects | Neural Stem Cells - metabolism | Retinal Ganglion Cells - drug effects | Stem Cells and Regeneration
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 8, p. e23899
The Wnt/beta-catenin signalling pathway shares a key component, beta-catenin, with the cadherin-based adhesion system. The signalling function of beta-catenin... 
TYROSINE PHOSPHORYLATION | WNT PATHWAY | DEPENDENT TRANSCRIPTION | FACTOR SCATTER FACTOR | BIOLOGY | TUMOR-SUPPRESSOR PROTEIN | ADHERENS JUNCTIONS | BETA-CATENIN | CELL-CELL ADHESION | NUCLEAR TRANSLOCATION | N-CADHERIN | Embryo, Mammalian - drug effects | Transcription, Genetic - drug effects | Epithelial Cells - metabolism | Cadherins - metabolism | Epithelial Cells - drug effects | Humans | Transcriptional Activation - drug effects | Mesoderm - drug effects | Cytoplasm - metabolism | Epithelial-Mesenchymal Transition - drug effects | Protein Transport - drug effects | Mesoderm - cytology | Epithelial-Mesenchymal Transition - genetics | Hepatocyte Growth Factor - pharmacology | Embryo, Mammalian - metabolism | Protein Binding - drug effects | HEK293 Cells | Cell Membrane - metabolism | Epithelial Cells - cytology | Cell Membrane - drug effects | Endocytosis - drug effects | beta Catenin - metabolism | Animals | Wnt Signaling Pathway - drug effects | Wnt Signaling Pathway - genetics | Dogs | Mesoderm - metabolism | Mice | Cytoplasm - drug effects | Regulators | Phosphorylation | Wnt protein | Transcription | Mesenchyme | Colorectal cancer | Activation | Biology | Cell adhesion & migration | Signal transduction | β-catenin | Embryogenesis | Endocytosis | Cell growth | Tumorigenesis | Trends | Growth factors | Chromosomes | Medical research | Gastrulation | Hepatocyte growth factor | Gene expression | Cadherin | Adhesion | Embryonic growth stage | Signaling | Insects | Morphology | Stem cells | Ligands | Mutation | Endoplasmic reticulum | Cytoplasm
Journal Article
Cell Stem Cell, ISSN 1934-5909, 08/2010, Volume 7, Issue 2, pp. 225 - 239
Journal Article
Cell Stem Cell, ISSN 1934-5909, 2009, Volume 5, Issue 3, pp. 298 - 309
Journal Article
Blood, ISSN 0006-4971, 03/2013, Volume 121, Issue 10, pp. 1824 - 1838
Tyrosine kinase inhibitors (TKIs) are highly effective in treatment of chronic myeloid leukemia (CML) but do not eliminate leukemia stemcells (LSCs), which... 
ADHESION | IMATINIB | NICHE | FIBRONECTIN | RESISTANCE | STABILIZES | HEMATOLOGY | UP-REGULATION | EXPRESSION | CHRONIC MYELOID-LEUKEMIA | REMISSION | Cadherins - metabolism | Oligonucleotide Array Sequence Analysis | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Tumor Microenvironment | Drug Resistance, Neoplasm | Gene Expression Profiling | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Mesenchymal Stem Cells - drug effects | Biomarkers, Tumor - metabolism | Neoplastic Stem Cells - pathology | Phosphorylation - drug effects | Tumor Cells, Cultured | Cadherins - genetics | Real-Time Polymerase Chain Reaction | Bone Marrow - drug effects | RNA, Messenger - genetics | Reverse Transcriptase Polymerase Chain Reaction | beta Catenin - metabolism | Blotting, Western | beta Catenin - genetics | Mesenchymal Stem Cells - pathology | Fusion Proteins, bcr-abl - genetics | Animals | Mice, Nude | Bone Marrow - pathology | Fusion Proteins, bcr-abl - antagonists & inhibitors | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Biomarkers, Tumor - genetics | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Cell Cycle - drug effects | Fusion Proteins, bcr-abl - metabolism | Myeloid Neoplasia
Journal Article