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Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2013, Volume 110, Issue 10, pp. 4039 - 4044
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2010, Volume 107, Issue 13, pp. 6064 - 6069
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 04/2015, Volume 125, Issue 4, pp. 1433 - 1445
Oxidative stress contributes to the loss of neurons in many disease conditions as well as during normal aging; however, small-molecule agents that reduce... 
RETINAL DEGENERATION | MEDICINE, RESEARCH & EXPERIMENTAL | DIFFUSIBLE FACTOR | OXIDATIVE STRESS | OPTIC-NERVE | PLACEBO-CONTROLLED PHASE-3 | MOUSE MODEL | AXON REGENERATION | PARTIAL RECOVERY | RETINITIS-PIGMENTOSA | CONE CELL-DEATH | NF-E2-Related Factor 2 - physiology | Dependovirus - genetics | Genetic Therapy | Catalase - therapeutic use | NF-E2-Related Factor 2 - therapeutic use | Oxidative Stress - physiology | Genetic Vectors - therapeutic use | Mice, Mutant Strains | Superoxide Dismutase - physiology | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Neurons - physiology | NF-E2-Related Factor 2 - genetics | Optic Nerve Injuries - therapy | Transcription Factors - therapeutic use | Retinal Ganglion Cells - physiology | Transcription Factors - physiology | Catalase - physiology | Mice, Inbred C57BL | Optic Nerve Injuries - physiopathology | Nerve Crush | Retinal Cone Photoreceptor Cells - physiology | Genetic Vectors - genetics | Superoxide Dismutase - therapeutic use | Animals | Retinitis Pigmentosa - therapy | Mice | Nerve Degeneration | Apoptosis | Oxidative stress | Transcription factors | Nervous system | Development and progression | Degeneration | Genetic aspects | Health aspects | Antioxidants | Proteins | Enzymes | Statistical analysis | Optic nerve | Disease | Genes | Lipids | Photoreceptors | Physiology | Genetics | Neuroscience | Ophthalmology | Therapeutics
Journal Article
Cell Death and Disease, ISSN 2041-4889, 2014, Volume 5, Issue 5, pp. e1225 - e1225
The Rho/ROCK/LIMK pathway is central for the mediation of repulsive environmental signals in the central nervous system. Several studies using pharmacological... 
Regeneration | Retinal ganglion cells | ROCK2 | Axonal degeneration | Optic nerve crush | LIMK1 | APOPTOSIS | RHO-KINASE INHIBITION | SIGNALING PATHWAYS | ACTIVATION | regeneration | PHOSPHORYLATION | LIM-KINASE | axonal degeneration | optic nerve crush | CELL BIOLOGY | RETINAL GANGLION-CELLS | NEURITE OUTGROWTH | IN-VIVO | GROWTH | retinal ganglion cells | Dependovirus - genetics | Optic Nerve - pathology | Phosphorylation | Axons - enzymology | Calpain - metabolism | Rats, Wistar | Neurites - enzymology | Caspase 3 - metabolism | Autophagy | Gene Knockdown Techniques | Lim Kinases - metabolism | Retinal Ganglion Cells - pathology | Intercellular Signaling Peptides and Proteins - metabolism | Transfection | RNA Interference | Time Factors | rho-Associated Kinases - metabolism | Cell Death | Female | Optic Nerve Injuries - pathology | Optic Nerve - physiopathology | Proto-Oncogene Proteins c-akt - metabolism | Disease Models, Animal | Gene Transfer Techniques | Optic Nerve - enzymology | Retinal Ganglion Cells - enzymology | Signal Transduction | Optic Nerve Injuries - physiopathology | Cells, Cultured | Nerve Crush | Rats | rho-Associated Kinases - genetics | Nerve Regeneration | Nerve Tissue Proteins - metabolism | Neurites - pathology | Optic Nerve Injuries - enzymology | Optic Nerve Injuries - genetics | Animals | Axons - pathology | Lim Kinases - genetics | Genetic Vectors | Nerve Degeneration | Apoptosis | Original
Journal Article
Neuron, ISSN 0896-6273, 2009, Volume 64, Issue 5, pp. 617 - 623
Axon regeneration failure accounts for permanent functional deficits following CNS injury in adult mammals. However, the underlying mechanisms remain elusive.... 
MOLNEURO | SIGNALING | SURVIVAL | RETINAL GANGLION-CELLS | SIGNALING PATHWAYS | STIMULATES AXON REGENERATION | GROWTH | LEUKEMIA INHIBITORY FACTOR | SPINAL-CORD-INJURY | NEUROSCIENCES | SENSORY NEURONS | ADULT | TRANSGENIC MICE | Nerve Regeneration - physiology | Green Fluorescent Proteins - genetics | Suppressor of Cytokine Signaling Proteins - deficiency | Retinal Ganglion Cells - pathology | Dose-Response Relationship, Drug | Tubulin - metabolism | Time Factors | Ciliary Neurotrophic Factor - genetics | Ciliary Neurotrophic Factor - pharmacology | Organ Culture Techniques | Disease Models, Animal | Optic Nerve Injuries - drug therapy | Animals, Newborn | Nerve Regeneration - genetics | Retinal Ganglion Cells - physiology | Cholera Toxin - metabolism | Gene Expression Regulation - genetics | Mice, Inbred C57BL | Optic Nerve Injuries - physiopathology | Axons - drug effects | Axons - metabolism | Mice, Transgenic | Cytokine Receptor gp130 - deficiency | Phosphotransferases (Alcohol Group Acceptor) - metabolism | Optic Nerve Injuries - genetics | Suppressor of Cytokine Signaling 3 Protein | Animals | Carrier Proteins - metabolism | Analysis of Variance | Axons - pathology | Nerve Regeneration - drug effects | Suppressor of Cytokine Signaling Proteins - physiology | Mice | TOR Serine-Threonine Kinases | Injections, Intraventricular - methods | Neurosciences | Ciliary neurotrophic factor | Peptide hormones | Neurons | Analysis | Proteins | Studies | Medical research | Optic nerve | Rodents | Mammals | Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 12/2015, Volume 35, Issue 48, pp. 15934 - 15947
Journal Article
Neuron, ISSN 0896-6273, 02/2012, Volume 73, Issue 3, pp. 445 - 452
Loss of retinal ganglion cells (RGCs) accounts for visual function deficits after optic nerve injury, but how axonal insults lead to neuronal death remains... 
OPEN-ANGLE GLAUCOMA | OXIDATIVE STRESS | OPTIC-NERVE | MESSENGER-RNA | ER STRESS | TRANSCRIPTION FACTOR XBP-1 | OCULAR HYPERTENSION | ENDOPLASMIC-RETICULUM | RETINITIS-PIGMENTOSA | NEUROSCIENCES | MOUSE MODELS | Glaucoma - etiology | Axotomy - methods | Dependovirus - genetics | Caspase 3 - metabolism | Cell Survival - genetics | Green Fluorescent Proteins - genetics | RNA, Messenger - metabolism | X-Box Binding Protein 1 | Retinal Ganglion Cells - pathology | DNA-Binding Proteins - metabolism | Tubulin - metabolism | Flow Cytometry | Cell Death - genetics | Optic Nerve Injuries - pathology | Glaucoma - physiopathology | Gene Expression Regulation - genetics | Optic Nerve Injuries - etiology | Mice, Inbred C57BL | Optic Nerve Injuries - physiopathology | Gene Expression Regulation - physiology | Rats | Transcription Factor CHOP - deficiency | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Rats, Sprague-Dawley | Regulatory Factor X Transcription Factors | Amino Acids | Protein Folding | Mice, Knockout | Transcription Factors - metabolism | Animals | Mice | Glaucoma - genetics | Medical colleges | Neurons | Cell death | Analysis | Ophthalmology | Ganglion | Public health | Protein binding | Phosphorylation | Transcription factors | Optic nerve | Protein folding | Rodents | Hypoxia | Hybridization | Kinases | Apoptosis
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 11/2009, Volume 29, Issue 45, pp. 14334 - 14341
Journal Article
PLoS ONE, ISSN 1932-6203, 06/2014, Volume 9, Issue 6, p. e99299
Objective: To investigate the effect of molecular hydrogen (H-2) in a rat model subjected to optic nerve crush (ONC). Methods: We tested the hypothesis that... 
PUPILLARY LIGHT REFLEX | APOPTOSIS | REDUCING OXIDATIVE STRESS | ISCHEMIA/REPERFUSION INJURY | MICROGLIA | GLUTAMATE | MULTIDISCIPLINARY SCIENCES | MICE | PARKINSONS-DISEASE | FREE-RADICALS | PROTECTS | In Situ Nick-End Labeling | Malondialdehyde - metabolism | Cell Survival - drug effects | Hydrogen - pharmacology | Sodium Chloride - pharmacology | Cell Count | Optic Nerve Injuries - physiopathology | Nerve Crush | Reflex - drug effects | Male | Reflex - radiation effects | Rats, Sprague-Dawley | Retinal Ganglion Cells - pathology | Animals | Evoked Potentials, Visual - drug effects | gamma-Synuclein - metabolism | Pupil - radiation effects | Light | Staining and Labeling | Pupil - drug effects | Optic Nerve Injuries - pathology | Retinal Ganglion Cells - drug effects | Disease Models, Animal | Models | Cholera toxin | Ganglion | Hydrogen | Water-borne diseases | Neuroprotection | Oxidative stress | Spinal cord | Staining | Retina | Visual evoked potentials | Infections | Synuclein | Visual perception | Antioxidants | Ischemia | Rodents | Gangrene | Hydrogen ion concentration | Public health | Medical research | Optic nerve | Cell survival | Rats | Survival | Fatty acids | Malondialdehyde | Crush tests | DNA nucleotidylexotransferase | Medicine | Studies | Retinal ganglion cells | Cholera | Laboratory animals | Apoptosis
Journal Article