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Journal Article
PLoS ONE, ISSN 1932-6203, 04/2009, Volume 4, Issue 4, pp. e5388 - e5388
Background: Understanding how the mechanical microenvironment influences cell fate, and more importantly, by what molecular mechanisms, will enhance not only... 
MULTIDISCIPLINARY SCIENCES | RNA, Small Interfering - genetics | Osteogenesis - physiology | Cadherins - metabolism | Stress, Mechanical | Receptor Tyrosine Kinase-like Orphan Receptors | Wnt-5a Protein | Wnt Proteins - metabolism | Adherens Junctions - metabolism | Mesenchymal Stromal Cells - cytology | Wnt Proteins - genetics | Base Sequence | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Cell Differentiation | Cell Line | Signal Transduction | Mesenchymal Stromal Cells - metabolism | Receptor Protein-Tyrosine Kinases - metabolism | beta Catenin - metabolism | Biomechanical Phenomena | Animals | Receptor Protein-Tyrosine Kinases - genetics | Models, Biological | rho GTP-Binding Proteins - metabolism | Mice | Wnt Proteins - antagonists & inhibitors | Bioengineering | Transcription factors | Phosphorylation | Wnt protein | Transcription | Mesenchyme | Fluid flow | Homeostasis | Kinases | Regeneration (physiology) | Cell adhesion & migration | Proteins | β-catenin | Osteoporosis | Signal transduction | N-Cadherin | Cell fate | Loading | Biocompatibility | Bones | Bone density | Localization | Translocation | Heparan sulfate | Wound healing | Fluid dynamics | RhoA protein | Cadherin | Nuclear transport | Polymerase chain reaction | Regeneration | Molecular modelling | Morphology | Stem cells | Transduction | Bone | Mechanical stimuli | Mutation | Differentiation | Guanosinetriphosphatase | Index Medicus
Journal Article
Neuro-Oncology, ISSN 1522-8517, 02/2013, Volume 15, Issue 2, pp. 161 - 171
Background. Glioblastoma (GBM) is the most lethal and common type of primary brain tumor. Recent evidence suggests that a subpopulation of GBM cells... 
Glioblastoma stem cell | Wnt/bcatenin signaling | MET protooncogene | Hepatocyte growth factor | Glioblastoma | ACTIVATION | CARCINOMA CELLS | glioblastoma stem cell | Wnt/beta-catenin signaling | BETA-CATENIN | CLINICAL NEUROLOGY | TUMOR-INITIATING CELLS | BRAIN-TUMORS | BREAST-CANCER | GROWTH-FACTOR RECEPTOR | glioblastoma | EPITHELIAL-CELLS | ONCOLOGY | hepatocyte growth factor | C-MET | GENE-EXPRESSION | Proto-Oncogene Proteins c-met - metabolism | Cell Proliferation | Luciferases - metabolism | Oligonucleotide Array Sequence Analysis | Humans | Brain Neoplasms - pathology | Gene Expression Profiling | Brain Neoplasms - metabolism | Immunoenzyme Techniques | Glioblastoma - genetics | Neoplastic Stem Cells - metabolism | Biomarkers, Tumor - metabolism | Neoplastic Stem Cells - pathology | Glioblastoma - metabolism | Tumor Cells, Cultured | Real-Time Polymerase Chain Reaction | Wnt Signaling Pathway | Tumor Stem Cell Assay | Proto-Oncogene Proteins c-met - antagonists & inhibitors | RNA, Messenger - genetics | Brain Neoplasms - genetics | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Proto-Oncogene Proteins c-met - genetics | Xenograft Model Antitumor Assays | Animals | Mice, Nude | Glioblastoma - pathology | Biomarkers, Tumor - genetics | Mice | Apoptosis | Index Medicus | Basic and Translational Investigations | β-catenin signaling | Wnt
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 08/2017, Volume 21, Issue 8, pp. 1545 - 1554
Fibrosis in animal models and human diseases is associated with aberrant activation of the Wnt/β‐catenin pathway. Despite extensive research efforts, effective... 
Smad2/3 | myofibroblast proliferation | pulmonary fibrosis | Wnt/β‐catenin | Wnt/β-catenin | MEDICINE, RESEARCH & EXPERIMENTAL | TGF-BETA | MECHANISMS | BETA-CATENIN | PROTEIN CBP | CELL BIOLOGY | EPITHELIAL-MESENCHYMAL TRANSITION | PATHOGENESIS | INHIBITION | PATHWAY | Wnt/beta-catenin | IDIOPATHIC PULMONARY-FIBROSIS | PROMOTE | Cell Proliferation | Cadherins - metabolism | Vimentin - metabolism | Humans | Transforming Growth Factor beta1 - metabolism | Actins - metabolism | Smad3 Protein - metabolism | Wnt Proteins - metabolism | Actins - genetics | Myofibroblasts - metabolism | Smad3 Protein - genetics | Collagen Type I - genetics | Wnt Proteins - genetics | Vimentin - genetics | Smad2 Protein - genetics | Epithelial-Mesenchymal Transition | Cadherins - genetics | Fibroblasts - metabolism | A549 Cells | Cell Line | Myofibroblasts - pathology | Collagen Type I - metabolism | Signal Transduction | Gene Expression Regulation | Smad2 Protein - metabolism | Rats | Transforming Growth Factor beta1 - genetics | Fibroblasts - pathology | Rats, Sprague-Dawley | beta Catenin - metabolism | beta Catenin - genetics | Animals | Fibrosis | Vimentin | Animal models | Collagen (type I) | Wnt protein | Mesenchyme | Pathogenesis | Transforming growth factor-b | Lung | Activation | Proteins | β-catenin | Signal transduction | Molecular modelling | Smad2 protein | Effectors | Fibroblasts | Extracellular matrix | Autocrine signalling | Aberration | Index Medicus | Smad2 | β‐catenin | Wnt | Original
Journal Article
STEM CELLS, ISSN 1066-5099, 11/2016, Volume 34, Issue 11, pp. 2635 - 2647
As known from model organisms, such as frog, fish, mouse, and chicken, the anterior–posterior patterning of the definitive endoderm (DE) into distinct domains... 
Human embryonic stem cells | Pancreatic duodenal endoderm | Anterior‐posterior patterning | Differentiation | Definitive endoderm | Anterior-posterior patterning | ORGAN FORMATION | ZEBRAFISH | VIVO | FOREGUT ENDODERM | ACTIVIN | CELL & TISSUE ENGINEERING | CELL BIOLOGY | Anteriorposterior patterning | MORPHOGENESIS | IN-VITRO | XENOPUS | ONCOLOGY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | PANCREATIC PROGENITORS | HEMATOLOGY | EXPRESSION | Hepatocyte Nuclear Factor 3-beta - genetics | Bone Morphogenetic Protein 4 - genetics | Homeodomain Proteins - metabolism | Human Embryonic Stem Cells - cytology | Humans | Fibroblast Growth Factor 2 - pharmacology | Mesoderm - drug effects | Activins - metabolism | Mesoderm - cytology | Bone Morphogenetic Protein 4 - metabolism | Wnt3 Protein - genetics | SOXB1 Transcription Factors - metabolism | Immunomagnetic Separation | SOXB1 Transcription Factors - genetics | Endoderm - cytology | Gene Expression Regulation, Developmental | Human Embryonic Stem Cells - drug effects | Trans-Activators - genetics | Fibroblast Growth Factor 2 - metabolism | Wnt3 Protein - metabolism | Cell Differentiation | Wnt Signaling Pathway | Tretinoin - pharmacology | Hepatocyte Nuclear Factor 3-beta - metabolism | Cell Line | Human Embryonic Stem Cells - metabolism | beta Catenin - metabolism | Bone Morphogenetic Protein 4 - pharmacology | Homeodomain Proteins - genetics | beta Catenin - genetics | Endoderm - metabolism | Wnt3 Protein - pharmacology | Transforming Growth Factor beta - pharmacology | Transforming Growth Factor beta - genetics | Activins - pharmacology | Fibroblast Growth Factor 2 - genetics | Endoderm - drug effects | Trans-Activators - metabolism | Activins - genetics | Mesoderm - metabolism | Body Patterning - genetics | Transforming Growth Factor beta - metabolism | Bone morphogenetic proteins | Transforming growth factors | Embryonic stem cells | Analysis | Tretinoin | Embryos | Rodents | Stem cells | Pattern formation | Fibroblast growth factor | Wnt protein | Embryo cells | Mesoderm | Stem cell transplantation | Organisms | CDX2 protein | β-catenin | Inhibition | Pancreas | Endoderm | trans-Retinoic acid | Fibroblast growth factor 2 | Bone morphogenetic protein 4 | Inhibitors | Acids | Ligands | Activin | Retinoic acid | Foregut | Pluripotency | Index Medicus
Journal Article
Development, ISSN 0950-1991, 09/2006, Volume 133, Issue 18, pp. 3695 - 3707
Both the Wnt/beta-catenin and Ihh signaling pathways play essential roles in crucial aspects of endochondral ossification: osteoblast differentiation,... 
β-catenin | Cartilage | Chondrocyte hypertrophy | Ihh | Endochondral bone | Joint | Wnt | Patched | Osteoblast differentiation | beta-catenin | PATHWAYS | OSTEOBLAST | joint | PROTEIN | cartilage | chondrocyte hypertrophy | endochondral bone | PROLIFERATION | DEVELOPMENTAL BIOLOGY | CHONDROCYTE DIFFERENTIATION | SKELETON | osteoblast differentiation | patched | INDIAN-HEDGEHOG | PTH/PTHRP RECEPTOR | GROWTH-PLATE | Immunohistochemistry | Cell Cycle - genetics | Chondrocytes - cytology | Osteogenesis - physiology | Cell Proliferation | Cell Survival - genetics | Apoptosis - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Wnt Proteins - metabolism | Hedgehog Proteins | Cell Differentiation - genetics | In Situ Hybridization | Gene Expression Regulation, Developmental | Bone and Bones - metabolism | Cartilage - cytology | Receptors, Cell Surface - physiology | Osteoblasts - cytology | Patched Receptors | Cell Differentiation - physiology | Cell Survival - physiology | Chondrocytes - metabolism | Joints - metabolism | Osteogenesis - genetics | Bone and Bones - cytology | Cartilage - embryology | Receptors, Cell Surface - metabolism | In Situ Nick-End Labeling - methods | Signal Transduction - genetics | Cartilage - metabolism | Wnt Proteins - chemistry | beta Catenin - metabolism | beta Catenin - genetics | Chondrocytes - enzymology | Animals | Joints - embryology | Joints - cytology | Cell Cycle - physiology | Signal Transduction - physiology | Mice | Apoptosis - physiology | Bone and Bones - embryology | Osteoblasts - metabolism | Patched-1 Receptor | Receptors, Cell Surface - genetics | Index Medicus
Journal Article
Journal Article
Nature communications, ISSN 2041-1723, 08/2019, Volume 10, Issue 1, pp. 3882 - 16
The β-catenin mutation is frequently observed in hepatoblastoma (HB), but the underlying mechanism by which Wnt/β-catenin signaling induces HB tumor formation... 
PROTEIN | GENE | MULTIDISCIPLINARY SCIENCES | GROWTH | CATENIN | ARCHITECTURE | DEGRADATION | CANCER | EXPRESSION | NUCLEAR TRANSLOCATION | ESTROGEN-RECEPTOR | Cell proliferation | Wnt protein | Liver | Estrogens | Menopause | Oligonucleotides | Antisense oligonucleotides | Event-related potentials | Breast cancer | Kinases | Gene expression | Yes-associated protein | β-catenin | Signaling | Depletion | Smad2 protein | Mice | Tumorigenesis | Mutation | Tumors | Index Medicus
Journal Article