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Neuron, ISSN 0896-6273, 2003, Volume 40, Issue 3, pp. 485 - 499
The CNS is thought to develop from self-renewing stem cells that generate neurons, astrocytes, and oligodendrocytes. Other data, however, have suggested that... 
OLIGODENDROCYTE LINEAGE | PROGENITOR CELLS | TRANSCRIPTION FACTORS | GLIAL-RESTRICTED PRECURSORS | RAT CEREBRAL-CORTEX | SONIC HEDGEHOG | EMBRYONIC SPINAL-CORD | NEURAL-TUBE | CENTRAL-NERVOUS-SYSTEM | MAMMALIAN FOREBRAIN | NEUROSCIENCES | Immunohistochemistry | Green Fluorescent Proteins | O Antigens - metabolism | Embryo, Mammalian | Cell Count | Homeodomain Proteins - metabolism | Fibroblast Growth Factor 2 - pharmacology | Glial Fibrillary Acidic Protein - metabolism | Hedgehog Proteins | RNA, Messenger - biosynthesis | Time Factors | SOXE Transcription Factors | Neurons - metabolism | Basic Helix-Loop-Helix Transcription Factors | Receptor, Platelet-Derived Growth Factor alpha - metabolism | Enzyme Inhibitors - pharmacology | Proteoglycans - metabolism | Rats | Oligodendrocyte Transcription Factor 2 | Mice | Astrocytes - metabolism | Oligodendroglia - metabolism | Flow Cytometry - methods | Epithelial Cells - metabolism | Epithelial Cells - drug effects | PAX7 Transcription Factor | Carbocyanines - metabolism | DNA-Binding Proteins - metabolism | Dose-Response Relationship, Drug | Tubulin - metabolism | Transfection | Reverse Transcriptase Polymerase Chain Reaction - methods | beta-Galactosidase - metabolism | Fibroblast Growth Factor 2 - physiology | Bromodeoxyuridine - metabolism | Spinal Cord - cytology | Cell Differentiation - physiology | High Mobility Group Proteins - metabolism | Cells, Cultured | Antigens - metabolism | Body Patterning - physiology | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Spinal Cord - embryology | Blotting, Northern | Animals | Cell Aggregation | Stem Cells - physiology | Trans-Activators - metabolism | Epidermal Growth Factor - pharmacology | In Vitro Techniques | Luminescent Proteins - metabolism | Spinal cord | Scholarships & fellowships | Neurosciences | Rodents | Stem cells | Experiments | Neurogenesis | Index Medicus
Journal Article
Plant Physiology, ISSN 0032-0889, 11/2015, Volume 169, Issue 3, pp. 2048 - 2063
Journal Article
Aging Cell, ISSN 1474-9718, 08/2017, Volume 16, Issue 4, pp. 837 - 846
Kallistatin, an endogenous protein, protects against vascular injury by inhibiting oxidative stress and inflammation in hypertensive rats and enhancing the... 
34a | sirtuin 1 | RNA | micro | kallistatin | vascular senescence | aging | oxidative stress | microRNA-34a | NECROSIS-FACTOR-ALPHA | TISSUE KALLIKREIN INHIBITOR | BINDING PROTEIN | CELL BIOLOGY | GERIATRICS & GERONTOLOGY | ORGAN INJURY | CAENORHABDITIS-ELEGANS | PROTECTIVE ROLE | PROGENITOR-CELL SENESCENCE | ENDOTHELIAL-CELLS | RENAL INJURY | Sirtuin 1 - metabolism | Diabetes Mellitus, Experimental - drug therapy | Endothelial Progenitor Cells - cytology | MicroRNAs - antagonists & inhibitors | Streptozocin | Humans | Diabetes Mellitus, Experimental - genetics | NADPH Oxidases - metabolism | Caenorhabditis elegans Proteins - metabolism | Cellular Senescence - drug effects | Male | MicroRNAs - metabolism | Sirtuin 1 - genetics | Telomerase - genetics | Plasminogen Activator Inhibitor 1 - metabolism | Superoxides - metabolism | beta-Galactosidase - metabolism | NADPH Oxidases - genetics | Telomerase - metabolism | Diabetes Mellitus, Experimental - chemically induced | Superoxides - antagonists & inhibitors | Nitric Oxide Synthase Type III - metabolism | Plasminogen Activator Inhibitor 1 - genetics | Diabetes Mellitus, Experimental - metabolism | Sirtuins - genetics | Endothelial Progenitor Cells - metabolism | Cellular Senescence - genetics | Caenorhabditis elegans - metabolism | Caenorhabditis elegans - genetics | Catalase - genetics | Endothelial Progenitor Cells - drug effects | Cells, Cultured | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Nitric Oxide Synthase Type III - genetics | Serpins - pharmacology | Catalase - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Animals | Caenorhabditis elegans - drug effects | Genistein - pharmacology | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Mice | MicroRNAs - genetics | beta-Galactosidase - genetics | Caenorhabditis elegans Proteins - genetics | Sirtuins - metabolism | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Gene expression | MicroRNA | Oxidative stress | Senescence | Genistein | INK4a protein | Kinases | NAD(P)H oxidase | Catalase | Rodents | Aging | Aorta | Telomerase | Protein-tyrosine kinase | Tyrosine | Enzymes | Diabetes mellitus | p16 Protein | MiRNA | Superoxide | SIRT1 protein | Life span | Tumor necrosis factor | MicroRNAs | Stem cells | Nematodes | Diabetes | Index Medicus | microRNA‐34a | Original
Journal Article
Nature Neuroscience, ISSN 1097-6256, 11/2004, Volume 7, Issue 11, pp. 1233 - 1241
Establishing the cellular identity in vivo of adult multipotent neural progenitors is fundamental to understanding their biology. We used two transgenic... 
SITE-SPECIFIC RECOMBINATION | NEURAL STEM-CELLS | RADIAL GLIAL-CELLS | FIBRILLARY ACIDIC PROTEIN | IN-VIVO | CENTRAL-NERVOUS-SYSTEM | SUBVENTRICULAR ZONE | MAMMALIAN FOREBRAIN | NEUROSCIENCES | INTERMEDIATE-FILAMENT PROTEIN | TRANSGENIC MICE | Glial Fibrillary Acidic Protein - genetics | Microtubule-Associated Proteins - metabolism | Phosphopyruvate Hydratase - metabolism | Prosencephalon - physiology | Olfactory Bulb - metabolism | Hippocampus - drug effects | Glial Fibrillary Acidic Protein - metabolism | Prosencephalon - drug effects | Tubulin - metabolism | Neurons - physiology | beta-Galactosidase - metabolism | Ganciclovir - pharmacology | Integrases - metabolism | Bromodeoxyuridine - metabolism | Neural Cell Adhesion Molecule L1 - metabolism | Cell Differentiation - physiology | Olfactory Bulb - cytology | Green Fluorescent Proteins - metabolism | Thymidine Kinase - genetics | Neuroglia - physiology | Sialic Acids - metabolism | Gene Expression Regulation - physiology | Cell Size | Mice, Transgenic | Neuropeptides - metabolism | Hippocampus - cytology | Gene Expression Regulation - drug effects | Immunohistochemistry - methods | Hippocampus - metabolism | Animals | Cell Count - methods | Analysis of Variance | Cell Differentiation - drug effects | Prosencephalon - cytology | Stem Cells - drug effects | Stem Cells - physiology | Mice | Olfactory Bulb - drug effects | Physiological aspects | Brain | Cellular proteins | Research | Neurons | Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 01/2009, Volume 29, Issue 2, pp. 529 - 542
Aging may be determined by a genetic program and/or by the accumulation rate of molecular damages. Reactive oxygen species (ROS) generated by the mitochondrial... 
Aging | Antioxidant | Bmi1 | Neuronal cell death | ROS | p53 | antioxidant | OXIDATIVE-STRESS | STEM-CELLS | ACTIVATION | ALZHEIMERS-DISEASE | EXTENDS LIFE-SPAN | CELLULAR SENESCENCE | NEUROSCIENCES | neuronal cell death | IN-VIVO | INTRACELLULAR AMYLOID-BETA | aging | EXPRESSION | PARKINSONS-DISEASE | Cell Proliferation | Reactive Oxygen Species - metabolism | Age Factors | Embryo, Mammalian | Microtubule-Associated Proteins - metabolism | Homeodomain Proteins - metabolism | Peroxiredoxins - metabolism | Cell Survival - genetics | Apoptosis - genetics | Phosphopyruvate Hydratase - metabolism | Glial Fibrillary Acidic Protein - metabolism | Cerebral Cortex - cytology | Tumor Suppressor Protein p53 - genetics | Peroxiredoxins - genetics | Nuclear Proteins - deficiency | beta-Galactosidase - metabolism | Neurons - metabolism | Neurons - drug effects | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Gene Expression Regulation - genetics | Mice, Inbred C57BL | Cells, Cultured | Hydrogen Peroxide - pharmacology | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | PAX6 Transcription Factor | Proto-Oncogene Proteins - deficiency | Mice, Knockout | Neurotoxins - pharmacology | Animals | Polycomb Repressive Complex 1 | Analysis of Variance | Eye Proteins - metabolism | Mice | Histones - metabolism | Lipid Peroxidation - genetics | Paired Box Transcription Factors - metabolism | Index Medicus
Journal Article
American Journal of Obstetrics and Gynecology, ISSN 0002-9378, 2015, Volume 213, Issue 3, pp. 359.e1 - 359.e16
Journal Article
Cell Metabolism, ISSN 1550-4131, 2005, Volume 2, Issue 3, pp. 153 - 163
Journal Article
Scientific Reports, ISSN 2045-2322, 03/2016, Volume 6, Issue 1, pp. 23795 - 23795
We characterized cerebral Oil Red O-positive lipid-laden cells (LLC) of aging mice evaluating their distribution, morphology, density, functional activities... 
IN-VITRO | SECRETORY PHENOTYPE | WHITE-MATTER | AGE-RELATED-CHANGES | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | NEURAL STEM | SUBVENTRICULAR ZONE | PROINFLAMMATORY CYTOKINES | NEURODEGENERATIVE DISEASES | CEREBRAL-CORTEX | Tumor Necrosis Factor-alpha - metabolism | Glial Fibrillary Acidic Protein - genetics | Microglia - metabolism | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Cell Count | Tumor Necrosis Factor-alpha - genetics | Glial Fibrillary Acidic Protein - metabolism | Autophagy | Neurogenesis | Cerebral Cortex - metabolism | Meninges - metabolism | Cerebral Cortex - ultrastructure | Lipid Droplets - ultrastructure | Neurons - ultrastructure | beta-Galactosidase - metabolism | Female | S100 Calcium Binding Protein beta Subunit - genetics | Microfilament Proteins - metabolism | Neurons - metabolism | S100 Calcium Binding Protein beta Subunit - metabolism | Lipid Droplets - metabolism | Microfilament Proteins - genetics | Calcium-Binding Proteins - metabolism | Gene Expression | Astrocytes - ultrastructure | Phenotype | Animals | Perilipin-1 - genetics | Microglia - ultrastructure | Histocytochemistry | Beclin-1 - genetics | Mice | Mice, Inbred BALB C | Perilipin-1 - metabolism | beta-Galactosidase - genetics | Beclin-1 - metabolism | Meninges - ultrastructure | Aging - metabolism | Astrocytes - metabolism | Calcium-Binding Proteins - genetics | Senescence | Astrocytes | Glial fibrillary acidic protein | Cortex | Parenchyma | Blood vessels | Ventricles (cerebral) | Lipids | Inflammation | Neuronal-glial interactions | Microglia | Ependymal cells | Tumor necrosis factor | Neostriatum | Aging | Ventricle | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 8, pp. e23367 - e23367
Background: Recent studies have demonstrated that activation of autophagy increases the lifespan of organisms from yeast to flies. In contrast to the lifespan... 
LIFE-SPAN EXTENSION | LONGEVITY | OXIDATIVE STRESS | INHIBITION | LIPOFUSCIN | DISEASE | BIOLOGY | MITOCHONDRIAL DYSFUNCTION | C-ELEGANS | ADULT DROSOPHILA | CELL-DEATH | Reactive Oxygen Species - metabolism | TOR Serine-Threonine Kinases - metabolism | Sequestosome-1 Protein | Humans | Cellular Senescence - drug effects | Male | Autophagy - physiology | Phosphoproteins - metabolism | Fibroblasts - ultrastructure | Tumor Suppressor Protein p53 - genetics | Small Ubiquitin-Related Modifier Proteins - genetics | Toluene - analogs & derivatives | RNA Interference | Time Factors | beta-Galactosidase - metabolism | Autophagy - genetics | Toluene - pharmacology | Child | Fibroblasts - metabolism | Autophagy-Related Protein 12 | Cellular Senescence - genetics | Ubiquitin-Activating Enzymes - genetics | Lysosome-Associated Membrane Glycoproteins - metabolism | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Benzothiazoles - pharmacology | Small Ubiquitin-Related Modifier Proteins - metabolism | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Cellular Senescence - physiology | Signal Transduction - genetics | Microscopy, Electron | Ubiquitin-Activating Enzymes - metabolism | Blotting, Western | Autophagy-Related Protein 7 | Acetylcysteine - pharmacology | Lysosome-Associated Membrane Glycoproteins - genetics | Signal Transduction - physiology | Fibroblasts - cytology | Primary Cell Culture | Adaptor Proteins, Signal Transducing - metabolism | Lysosomal-Associated Membrane Protein 2 | Acetylcysteine | Tumor proteins | Genetic translation | Cells | Protein binding | TOR protein | Huntingtons disease | Senescence | Phosphorylation | Yeast | p53 Protein | Impairment | Galactosidase | Viruses | Homology | Activation | Biochemistry | Autophagy | Fibroblasts | Aging | Cytokines | LAMP-2 protein | Translation initiation | Rapamycin | Ribosomal protein S6 | siRNA | Mammals | Membrane proteins | Medicine | Life span | Morphology | Initiation factor eIF-4E | Molecular biology | Alzheimers disease | Phagocytosis | Apoptosis | Index Medicus
Journal Article
Nature Neuroscience, ISSN 1097-6256, 08/2011, Volume 14, Issue 8, pp. 1009 - 1016
Permanent damage to white matter tracts, comprising axons and myelinating oligodendrocytes, is an important component of brain injuries of the newborn that... 
FUNCTIONAL INTERACTION | MULTIPLE-SCLEROSIS | CNS REMYELINATION | MYELINATION | SIGNALING PATHWAY | TRANSCRIPTION | DIFFERENTIATION | BETA-CATENIN | NEUROSCIENCES | WHITE-MATTER INJURY | NEGATIVE REGULATOR | Humans | Ki-67 Antigen - metabolism | Male | Brain Injuries - metabolism | Wnt Proteins - metabolism | Oligodendroglia - drug effects | Hypoxia-Ischemia, Brain - therapy | Infant, Newborn | Organ Culture Techniques | Disease Models, Animal | Animals, Newborn | Basic Helix-Loop-Helix Transcription Factors - genetics | Mice, Transgenic | Oligodendrocyte Transcription Factor 2 | Brain Injuries - therapy | Multiple Sclerosis - therapy | Myelin Proteins - genetics | beta Catenin - metabolism | Heterocyclic Compounds, 3-Ring - therapeutic use | Spinal Cord - physiology | Axin Protein | Mice | Myelin Sheath - ultrastructure | beta-Galactosidase - genetics | Cerebellum - ultrastructure | Myelin Proteins - metabolism | Corpus Callosum - metabolism | Spinal Cord - drug effects | Heterocyclic Compounds, 3-Ring - pharmacology | Myelin Proteins - therapeutic use | Cerebellum - drug effects | Myelin Sheath - drug effects | Hypoxia-Ischemia, Brain - pathology | Cerebral Cortex - cytology | Cytoskeletal Proteins - deficiency | Dose-Response Relationship, Drug | Oligodendroglia - physiology | Wnt Proteins - genetics | beta-Galactosidase - metabolism | Adult | Cytoskeletal Proteins - metabolism | Female | Demyelinating Diseases - chemically induced | Demyelinating Diseases - pathology | Neurons - drug effects | Cell Differentiation - physiology | Hypoxia-Ischemia, Brain - metabolism | Microscopy, Electron, Transmission | Myelin Sheath - pathology | Gene Expression Regulation - genetics | Cerebellum - metabolism | Cells, Cultured | Gene Expression Regulation - physiology | Corpus Callosum - drug effects | Nerve Tissue Proteins - genetics | beta Catenin - genetics | Multiple Sclerosis - complications | Nerve Tissue Proteins - metabolism | Animals | Cell Differentiation - drug effects | Multiple Sclerosis - pathology | Stem Cells - drug effects | Brain Injuries - etiology | Lysophosphatidylcholines - toxicity | Postmortem Changes | Infants (Newborn) | Brain | Care and treatment | Physiological aspects | Research | Binding proteins | Health aspects | Injuries | Index Medicus
Journal Article