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Proceedings of the National Academy of Sciences, ISSN 0027-8424, 08/2011, Volume 108, Issue 32, pp. E440 - E449
Astrocytes regulate synaptic connectivity in the CNS through secreted signals. Here we identified two astrocyte-secreted proteins, hevin and SPARC, as... 
Extracellular matrix | Synaptic cleft 1 | Matricellular protein | Osteonectin | SPARC-Like | osteonectin | SC1 | synaptic cleft 1 | RAT | EXTRACELLULAR-MATRIX GLYCOPROTEIN | INTEGRIN | MULTIDISCIPLINARY SCIENCES | RECEPTOR | matricellular protein | CELL-SURVIVAL | SUPERIOR COLLICULUS | SPARC-Like 1 | EXPRESSION | extracellular matrix | SUPERFICIAL LAYERS | BRAIN | Central Nervous System - ultrastructure | Central Nervous System - metabolism | Extracellular Matrix Proteins - deficiency | Humans | Superior Colliculi - ultrastructure | Calcium-Binding Proteins - antagonists & inhibitors | Culture Media, Conditioned - pharmacology | Retinal Ganglion Cells - metabolism | Retinal Ganglion Cells - cytology | Osteonectin - deficiency | Synapses - metabolism | HEK293 Cells | Neurogenesis - drug effects | Extracellular Matrix Proteins - metabolism | Astrocytes - cytology | Calcium-Binding Proteins - chemistry | Calcium-Binding Proteins - metabolism | Protein Structure, Tertiary | Astrocytes - drug effects | Retinal Ganglion Cells - ultrastructure | Synapses - drug effects | Extracellular Matrix Proteins - chemistry | Superior Colliculi - metabolism | Extracellular Matrix Proteins - antagonists & inhibitors | Superior Colliculi - drug effects | Osteonectin - metabolism | Rats | Calcium-Binding Proteins - deficiency | Synapses - ultrastructure | Osteonectin - chemistry | Rats, Sprague-Dawley | Astrocytes - ultrastructure | Animals | Central Nervous System - cytology | Superior Colliculi - cytology | Mice | Retinal Ganglion Cells - drug effects | Astrocytes - secretion | Biological Sciences | PNAS Plus
Journal Article
Nature Genetics, ISSN 1061-4036, 11/2007, Volume 39, Issue 11, pp. 1338 - 1349
Many cancer-associated genes remain to be identified to clarify the underlying molecular mechanisms of cancer susceptibility and progression. Better... 
ZYG-9 FORM | COMPLEX | CAENORHABDITIS-ELEGANS | PROTEIN | AMPLIFICATION | GENETIC INSTABILITY | TAC-1 | GENETICS & HEREDITY | C-ELEGANS | BRCA1 | MUTATIONS | Oligonucleotide Array Sequence Analysis | Humans | Ubiquitin - metabolism | Gene Expression Profiling | Gene Regulatory Networks | Case-Control Studies | BRCA2 Protein - antagonists & inhibitors | BRCA1 Protein - metabolism | Hyaluronan Receptors - metabolism | Polymerase Chain Reaction | Biomarkers, Tumor - metabolism | Centrosome - physiology | Female | Extracellular Matrix Proteins - metabolism | Protein-Serine-Threonine Kinases - metabolism | Neural Networks (Computer) | Genetic Predisposition to Disease | Extracellular Matrix Proteins - antagonists & inhibitors | Extracellular Matrix Proteins - genetics | RNA, Small Interfering - pharmacology | Computational Biology | Protein-Serine-Threonine Kinases - genetics | Aurora Kinases | Hyaluronan Receptors - genetics | Protein Interaction Mapping | BRCA1 Protein - genetics | BRCA2 Protein - metabolism | Breast Neoplasms - genetics | BRCA1 Protein - antagonists & inhibitors | Biomarkers, Tumor - genetics | BRCA2 Protein - genetics | Complications and side effects | Gene mutations | Genes | Breast cancer | Genetic aspects | Research | Identification and classification | Risk factors | Genetic research | Models | Cellular biology | Gene expression | Genomics
Journal Article
Development (Cambridge), ISSN 0950-1991, 12/2017, Volume 144, Issue 23, pp. 4336 - 4349
Epithelia are bound by both basal and apical extracellular matrices (ECM). Although the composition and function of the former have been intensively... 
Apical extracellular matrix | C. elegans | Zona pellucid protein | Embryonic elongation | Laser nano-ablation | Muscle anchoring | STRUCTURAL-CHARACTERIZATION | DEVELOPMENTAL BIOLOGY | Zona pellucida protein | MASS-SPECTROMETRY | SHAPE | CAENORHABDITIS-ELEGANS | GENE | ELONGATION | EPITHELIAL MORPHOGENESIS | PELLUCIDA DOMAIN PROTEINS | EXTRACELLULAR-MATRIX | C.-ELEGANS | Genes, Helminth | Stress, Mechanical | Caenorhabditis elegans - physiology | Zona Pellucida Glycoproteins - genetics | RNA Interference | Extracellular Matrix - physiology | Actomyosin - physiology | Zona Pellucida Glycoproteins - physiology | Proteins - physiology | Morphogenesis - genetics | Caenorhabditis elegans - genetics | Extracellular Matrix Proteins - antagonists & inhibitors | Extracellular Matrix Proteins - genetics | Extracellular Matrix Proteins - physiology | Caenorhabditis elegans - embryology | Body Patterning - physiology | Proteins - genetics | Biomechanical Phenomena | Animals | Caenorhabditis elegans Proteins - antagonists & inhibitors | Models, Biological | Caenorhabditis elegans Proteins - physiology | Zona Pellucida Glycoproteins - antagonists & inhibitors | Body Patterning - genetics | Caenorhabditis elegans Proteins - genetics | Proteins - antagonists & inhibitors | Morphogenesis - physiology | Sheath proteins | Actomyosin | RNA-mediated interference | Muscles | p21-activated kinase | Epidermis | Leucine | Fibrillin | Embryos | Zona pellucida | Morphogenesis | Proteins | Nematodes | Extracellular matrix | Elongation | Life Sciences | Development Biology
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2014, Volume 9, Issue 8, p. e106155
A characteristic of dysregulated wound healing in IPF is fibroblastic-mediated damage to lung epithelial cells within fibroblastic foci. In these foci,... 
APOPTOSIS | COMPLEX | EFFICACY | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | TORC1/2 INHIBITOR | HYDROGEN-PEROXIDE | RICTOR | AKT | IDIOPATHIC PULMONARY-FIBROSIS | TRIPTOLIDE | Benzoxazoles - pharmacology | Epithelial Cells - metabolism | TOR Serine-Threonine Kinases - metabolism | Coculture Techniques | Epithelial Cells - drug effects | Multiprotein Complexes - genetics | Pulmonary Fibrosis - genetics | Mechanistic Target of Rapamycin Complex 2 | Proto-Oncogene Proteins c-akt - genetics | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | TOR Serine-Threonine Kinases - antagonists & inhibitors | Multiprotein Complexes - metabolism | Bleomycin | TOR Serine-Threonine Kinases - genetics | Protective Agents - pharmacology | Epithelial Cells - cytology | Proto-Oncogene Proteins c-akt - metabolism | Extracellular Matrix Proteins - metabolism | Fibroblasts - metabolism | Rapamycin-Insensitive Companion of mTOR Protein | Signal Transduction | Extracellular Matrix Proteins - antagonists & inhibitors | Extracellular Matrix Proteins - genetics | Carrier Proteins - antagonists & inhibitors | Gene Expression Regulation | Pulmonary Fibrosis - pathology | Pyrimidines - pharmacology | Fibroblasts - pathology | Carrier Proteins - genetics | Transforming Growth Factor beta - pharmacology | Animals | Carrier Proteins - metabolism | Fibroblasts - drug effects | Pulmonary Fibrosis - chemically induced | Mice | Pulmonary Fibrosis - drug therapy | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Bone morphogenetic proteins | Transforming growth factors | Lung diseases | Fibrosis | TOR protein | Cell culture | Phosphorylation | Transplants & implants | Pathogenesis | Epithelial cells | Critical care | AKT protein | Activation | Kinases | Cell adhesion & migration | Proteins | Cell cycle | Fibroblasts | Inhibition | Growth factors | Wound healing | Pulmonary arteries | Medical treatment | Metabolism | Medicine | Pulmonary fibrosis | Laboratory animals | Regulatory proteins
Journal Article
Cancer Research, ISSN 0008-5472, 02/2017, Volume 77, Issue 4, pp. 982 - 995
Journal Article
Scientific Reports, ISSN 2045-2322, 11/2015, Volume 5, Issue 1, p. 16985
Cancer cells acquire invasive ability to degrade and adhere to extracellular matrix (ECM) and migrate to adjacent tissues. This ultimately results metastasis.... 
MIGRATION | HEXAPEPTIDES | ANGIOGENESIS | CYCLIN D1 | RUBIA-YUNNANENSIS | PHOSPHORYLATION | CANCER METASTASIS | INTEGRIN | MULTIDISCIPLINARY SCIENCES | THERAPEUTIC TARGET | EXPRESSION | Urokinase-Type Plasminogen Activator - antagonists & inhibitors | Cyclins - genetics | Integrins - genetics | Mammary Neoplasms, Experimental - metabolism | Integrins - metabolism | Mammary Neoplasms, Experimental - genetics | Matrix Metalloproteinase 9 - metabolism | Cyclins - metabolism | Matrix Metalloproteinase 9 - genetics | Receptors, Chemokine - genetics | Cofilin 1 - antagonists & inhibitors | Cyclins - antagonists & inhibitors | Signal Transduction | Extracellular Matrix Proteins - antagonists & inhibitors | Extracellular Matrix Proteins - genetics | Lymphatic Metastasis | Cell Adhesion - drug effects | Cofilin 1 - genetics | Cell Movement - drug effects | Intercellular Adhesion Molecule-1 - metabolism | Cofilin 1 - metabolism | Urokinase-Type Plasminogen Activator - metabolism | Intercellular Adhesion Molecule-1 - genetics | Cell Line, Tumor | Mitogen-Activated Protein Kinases - genetics | Mice | Mice, Inbred BALB C | G1 Phase Cell Cycle Checkpoints - drug effects | Vascular Cell Adhesion Molecule-1 - metabolism | Integrins - antagonists & inhibitors | Gene Expression Regulation, Neoplastic | Peptides, Cyclic - pharmacology | Mammary Neoplasms, Experimental - pathology | Female | Vascular Cell Adhesion Molecule-1 - genetics | Receptors, Chemokine - antagonists & inhibitors | Extracellular Matrix Proteins - metabolism | Mammary Neoplasms, Experimental - drug therapy | Mammary Glands, Animal - pathology | Neoplasm Invasiveness | Receptors, Chemokine - metabolism | Mammary Glands, Animal - drug effects | Urokinase-Type Plasminogen Activator - genetics | Animals | Mammary Glands, Animal - metabolism | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Protein Binding | Cell Proliferation - drug effects | Antineoplastic Agents, Phytogenic - pharmacology | Mitogen-Activated Protein Kinases - metabolism | Leukocyte migration | AKT protein | Metastasis | Matrix metalloproteinase | Kinases | Fibronectin | Metastases | Cell adhesion molecules | Cell adhesion & migration | Angiogenesis | Laminin | Cofilin | Extracellular matrix | Metalloproteinase | G1 phase | NF-κB protein | Epidermal growth factor receptors | Invasiveness | MAP kinase | Breast cancer | Chemokine receptors | Cyclins | 1-Phosphatidylinositol 3-kinase | Collagen | Focal adhesion kinase | Cell migration | Tumors | Integrins
Journal Article