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Publication DateIEEE Microwave and Wireless Components Letters, ISSN 1531-1309, 07/2010, Volume 20, Issue 7, pp. 399 - 401
This letter presents a new symmetrical tail current-shaping technique to improve the phase noise of a quadrature voltage-controlled oscillator (QVCO). This...
Phase noise | LC oscillators | Energy consumption | tail current-shaping | Phase measurement | injection-locked oscillators (ILO) | Noise measurement | Radio frequency | Injection-locked oscillators | Voltage-controlled oscillators | Tail | Voltage | radio frequency (RF) | CMOS technology | CMOS integrated circuits | quadrature VCO (QVCO) | phase noise | OSCILLATORS | ENGINEERING, ELECTRICAL & ELECTRONIC | Integrated circuits | Digital broadcasting | Noise | CMOS | Electric potential | Oscillations | Current sources | Figure of merit | Oscillators | Quadratures
Phase noise | LC oscillators | Energy consumption | tail current-shaping | Phase measurement | injection-locked oscillators (ILO) | Noise measurement | Radio frequency | Injection-locked oscillators | Voltage-controlled oscillators | Tail | Voltage | radio frequency (RF) | CMOS technology | CMOS integrated circuits | quadrature VCO (QVCO) | phase noise | OSCILLATORS | ENGINEERING, ELECTRICAL & ELECTRONIC | Integrated circuits | Digital broadcasting | Noise | CMOS | Electric potential | Oscillations | Current sources | Figure of merit | Oscillators | Quadratures
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Loading RightsPLoS ONE, ISSN 1932-6203, 04/2012, Volume 7, Issue 4, p. e34693
LRRK2, a Parkinson's disease associated gene, is highly expressed in microglia in addition to neurons; however, its function in microglia has not been...
PARKIN DEFICIENCY INCREASES | TRANSCRIPTIONAL ACTIVITY | DNA-BINDING | IN-VITRO | ACTIVATED PROTEIN-KINASE | LRRK2 EXPRESSION | CULTURED RAT MICROGLIA | NITRIC-OXIDE SYNTHASE | BIOLOGY | NEURONAL TOXICITY | NF-KAPPA-B | Cell Line | Microglia - metabolism | Nitric Oxide Synthase Type II - biosynthesis | Protein-Serine-Threonine Kinases - genetics | NF-kappa B - metabolism | Gene Knockdown Techniques | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 | Brain - metabolism | Animals | MAP Kinase Kinase 4 - metabolism | Encephalitis - metabolism | Lipopolysaccharides - pharmacology | Interleukin-1beta - biosynthesis | Mice | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Tumor Necrosis Factor-alpha - biosynthesis | Protein-Serine-Threonine Kinases - metabolism | RNA | Tumor necrosis factor | Nitric oxide | Luciferase | Inflammation | B cells | Protein kinases | Mitogens | Brain | Biotechnology | Neurosciences | Phosphorylation | Parkinson's disease | Transcription | Genes | Parkinsons disease | Kinases | Inflammatory diseases | Lipopolysaccharides | Interleukin 6 | Neurodegeneration | Rodents | LRRK2 protein | Deoxyribonucleic acid--DNA | Movement disorders | NF-κB protein | Immunoglobulins | Neurodegenerative diseases | Cloning | MAP kinase | JNK protein | Pharmacology | Tumor necrosis factor-α | Gene expression | Nitric-oxide synthase | Mutants | Microglia | Medicine | Polymerase chain reaction | Brain research | Ribonucleic acids | Protein kinase | Mutation | Alzheimers disease | NF- Kappa B protein | c-Jun amino-terminal kinase | DNA | Interleukin 1 | Microenvironments | Tumor necrosis factor- alpha | Deoxyribonucleic acid
PARKIN DEFICIENCY INCREASES | TRANSCRIPTIONAL ACTIVITY | DNA-BINDING | IN-VITRO | ACTIVATED PROTEIN-KINASE | LRRK2 EXPRESSION | CULTURED RAT MICROGLIA | NITRIC-OXIDE SYNTHASE | BIOLOGY | NEURONAL TOXICITY | NF-KAPPA-B | Cell Line | Microglia - metabolism | Nitric Oxide Synthase Type II - biosynthesis | Protein-Serine-Threonine Kinases - genetics | NF-kappa B - metabolism | Gene Knockdown Techniques | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 | Brain - metabolism | Animals | MAP Kinase Kinase 4 - metabolism | Encephalitis - metabolism | Lipopolysaccharides - pharmacology | Interleukin-1beta - biosynthesis | Mice | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Tumor Necrosis Factor-alpha - biosynthesis | Protein-Serine-Threonine Kinases - metabolism | RNA | Tumor necrosis factor | Nitric oxide | Luciferase | Inflammation | B cells | Protein kinases | Mitogens | Brain | Biotechnology | Neurosciences | Phosphorylation | Parkinson's disease | Transcription | Genes | Parkinsons disease | Kinases | Inflammatory diseases | Lipopolysaccharides | Interleukin 6 | Neurodegeneration | Rodents | LRRK2 protein | Deoxyribonucleic acid--DNA | Movement disorders | NF-κB protein | Immunoglobulins | Neurodegenerative diseases | Cloning | MAP kinase | JNK protein | Pharmacology | Tumor necrosis factor-α | Gene expression | Nitric-oxide synthase | Mutants | Microglia | Medicine | Polymerase chain reaction | Brain research | Ribonucleic acids | Protein kinase | Mutation | Alzheimers disease | NF- Kappa B protein | c-Jun amino-terminal kinase | DNA | Interleukin 1 | Microenvironments | Tumor necrosis factor- alpha | Deoxyribonucleic acid
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Loading RightsJournal of Biological Chemistry, ISSN 0021-9258, 04/2003, Volume 278, Issue 17, pp. 14747 - 14752
Peroxisome proliferator-activated receptor (PPAR)-γ agonists are now emerging as therapeutic drugs for various inflammatory diseases. However, their molecular...
Protein Biosynthesis | Repressor Proteins | Suppressor of Cytokine Signaling 1 Protein | Suppressor of Cytokine Signaling Proteins | Neuroglia - drug effects | Janus Kinase 2 | Inflammation - metabolism | Inflammation - drug therapy | Prostaglandin D2 - analogs & derivatives | Proto-Oncogene Proteins | Phosphorylation - drug effects | Carrier Proteins - physiology | Proteins - physiology | DNA-Binding Proteins - antagonists & inhibitors | Anti-Inflammatory Agents - pharmacology | Carrier Proteins - biosynthesis | Rats | Receptors, Cytoplasmic and Nuclear - agonists | Rats, Sprague-Dawley | Janus Kinase 1 | Gene Expression Regulation - drug effects | Suppressor of Cytokine Signaling 3 Protein | Animals | Signal Transduction - drug effects | STAT1 Transcription Factor | Neuroglia - metabolism | Inflammation - prevention & control | Prostaglandin D2 - pharmacology | STAT3 Transcription Factor | Thiazoles - pharmacology | Trans-Activators - antagonists & inhibitors | Transcription Factors - agonists | Thiazolidinediones | Astrocytes - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors
Protein Biosynthesis | Repressor Proteins | Suppressor of Cytokine Signaling 1 Protein | Suppressor of Cytokine Signaling Proteins | Neuroglia - drug effects | Janus Kinase 2 | Inflammation - metabolism | Inflammation - drug therapy | Prostaglandin D2 - analogs & derivatives | Proto-Oncogene Proteins | Phosphorylation - drug effects | Carrier Proteins - physiology | Proteins - physiology | DNA-Binding Proteins - antagonists & inhibitors | Anti-Inflammatory Agents - pharmacology | Carrier Proteins - biosynthesis | Rats | Receptors, Cytoplasmic and Nuclear - agonists | Rats, Sprague-Dawley | Janus Kinase 1 | Gene Expression Regulation - drug effects | Suppressor of Cytokine Signaling 3 Protein | Animals | Signal Transduction - drug effects | STAT1 Transcription Factor | Neuroglia - metabolism | Inflammation - prevention & control | Prostaglandin D2 - pharmacology | STAT3 Transcription Factor | Thiazoles - pharmacology | Trans-Activators - antagonists & inhibitors | Transcription Factors - agonists | Thiazolidinediones | Astrocytes - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors
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Loading RightsNeurobiology of Disease, ISSN 0969-9961, 07/2019, Volume 127, pp. 482 - 491
Dysfunctional regulation of inflammation may contribute to the progression of neurodegenerative diseases. The results of this study revealed that DJ-1, a...
PGD2 | DJ-1 | Parkinson's disease | PTGDS | Brain inflammation
PGD2 | DJ-1 | Parkinson's disease | PTGDS | Brain inflammation
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Loading RightsNeurobiology of Disease, ISSN 0969-9961, 07/2019, Volume 127, p. 482
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6.
Full Text
LRRK2 G2019S mutation attenuates microglial motility by inhibiting focal adhesion kinase
Nature Communications, ISSN 2041-1723, 09/2015, Volume 6, Issue 1, p. 8255
In response to brain injury, microglia rapidly extend processes that isolate lesion sites and protect the brain from further injury. Here we report that...
FAK | DOMAIN | TYROSINE PHOSPHORYLATION | CELL-MIGRATION | PHOSPHATASE | MULTIDISCIPLINARY SCIENCES | IN-VIVO | PROTEIN-COUPLED RECEPTORS | PROLIFERATION | BRAIN | PARKINSONS-DISEASE | Microglia - metabolism | Phosphorylation | Immunoprecipitation | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Humans | Protein-Serine-Threonine Kinases - genetics | Rats | Mice, Transgenic | Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors | Blotting, Western | Cell Movement - genetics | Gene Knockdown Techniques | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 | Animals | Brain Injuries | HEK293 Cells | Mice | Mutation | Wound Healing - genetics | Protein-Serine-Threonine Kinases - metabolism
FAK | DOMAIN | TYROSINE PHOSPHORYLATION | CELL-MIGRATION | PHOSPHATASE | MULTIDISCIPLINARY SCIENCES | IN-VIVO | PROTEIN-COUPLED RECEPTORS | PROLIFERATION | BRAIN | PARKINSONS-DISEASE | Microglia - metabolism | Phosphorylation | Immunoprecipitation | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Humans | Protein-Serine-Threonine Kinases - genetics | Rats | Mice, Transgenic | Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors | Blotting, Western | Cell Movement - genetics | Gene Knockdown Techniques | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 | Animals | Brain Injuries | HEK293 Cells | Mice | Mutation | Wound Healing - genetics | Protein-Serine-Threonine Kinases - metabolism
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Loading RightsJournal of Neurochemistry, ISSN 0022-3042, 12/2010, Volume 115, Issue 5, pp. 1161 - 1171
Microglia are known to be a primary inflammatory cell type in the brain. However, microglial inflammatory responses are attenuated in the injured brain...
brain inflammation | brain injury | astrocytes | microglia | Astrocytes | Brain inflammation | Brain injury | Microglia | BIOCHEMISTRY & MOLECULAR BIOLOGY | INDUCTION | NEUROSCIENCES | CELL-DEATH | PIAS PROTEINS | INTERFERON-GAMMA | CULTURED RAT MICROGLIA | NITRIC-OXIDE | LIPOPOLYSACCHARIDE | ACTIVATED PROTEIN-KINASES | NF-KAPPA-B | EXPRESSION | L-Lactate Dehydrogenase - metabolism | Reactive Oxygen Species - metabolism | STAT Transcription Factors - metabolism | Culture Media, Conditioned - pharmacology | RNA, Messenger - metabolism | Cerebral Cortex - cytology | Hypoxia - metabolism | Intracellular Fluid - drug effects | Transfection - methods | Astrocytes - chemistry | Intracellular Fluid - metabolism | Animals, Newborn | Astrocytes - drug effects | Microglia - drug effects | Anti-Inflammatory Agents - pharmacology | Hydrogen Peroxide - pharmacology | Gene Expression Regulation - physiology | Rats | Rats, Sprague-Dawley | Gene Expression Regulation - drug effects | Electrophoretic Mobility Shift Assay - methods | Glucose - deficiency | Astrocytes - physiology | Oligonucleotides - metabolism | Animals | Interferon-gamma - pharmacology | Nitric Oxide Synthase Type II - metabolism | Brain | Medical colleges | Neurosciences | Messenger RNA | Anti-inflammatory drugs | Nitric oxide | Protein biosynthesis | Inflammation | Biological response modifiers | Injuries | Interferon gamma | Neurochemistry | Brain damage | Immunology | Cellular biology | Oxygen | Phosphorylation | Hydrogen peroxide | mRNA | Glucose | Nitric-oxide synthase | Nuclear transport | Promoters | gamma -Interferon
brain inflammation | brain injury | astrocytes | microglia | Astrocytes | Brain inflammation | Brain injury | Microglia | BIOCHEMISTRY & MOLECULAR BIOLOGY | INDUCTION | NEUROSCIENCES | CELL-DEATH | PIAS PROTEINS | INTERFERON-GAMMA | CULTURED RAT MICROGLIA | NITRIC-OXIDE | LIPOPOLYSACCHARIDE | ACTIVATED PROTEIN-KINASES | NF-KAPPA-B | EXPRESSION | L-Lactate Dehydrogenase - metabolism | Reactive Oxygen Species - metabolism | STAT Transcription Factors - metabolism | Culture Media, Conditioned - pharmacology | RNA, Messenger - metabolism | Cerebral Cortex - cytology | Hypoxia - metabolism | Intracellular Fluid - drug effects | Transfection - methods | Astrocytes - chemistry | Intracellular Fluid - metabolism | Animals, Newborn | Astrocytes - drug effects | Microglia - drug effects | Anti-Inflammatory Agents - pharmacology | Hydrogen Peroxide - pharmacology | Gene Expression Regulation - physiology | Rats | Rats, Sprague-Dawley | Gene Expression Regulation - drug effects | Electrophoretic Mobility Shift Assay - methods | Glucose - deficiency | Astrocytes - physiology | Oligonucleotides - metabolism | Animals | Interferon-gamma - pharmacology | Nitric Oxide Synthase Type II - metabolism | Brain | Medical colleges | Neurosciences | Messenger RNA | Anti-inflammatory drugs | Nitric oxide | Protein biosynthesis | Inflammation | Biological response modifiers | Injuries | Interferon gamma | Neurochemistry | Brain damage | Immunology | Cellular biology | Oxygen | Phosphorylation | Hydrogen peroxide | mRNA | Glucose | Nitric-oxide synthase | Nuclear transport | Promoters | gamma -Interferon
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Loading RightsGlia, ISSN 0894-1491, 02/2018, Volume 66, Issue 2, pp. 445 - 458
Defects in repair of damaged brain accumulate injury and contribute to slow‐developing neurodegeneration. Here, we report that a deficiency of DJ‐1, a...
Sox9 | Parkinson's disease | astrogliosis | brain repair | DJ‐1 | DJ-1 | SYSTEM | PROTEIN | SPINAL-CORD | NEUROSCIENCES | DEGENERATION | PINK1 | GDNF | ROLES | NEURONS | REACTIVE ASTROCYTES | EXPRESSION | SOX9 Transcription Factor - metabolism | Gliosis - genetics | Gliosis - metabolism | Mice, Inbred C57BL | Astrocytes - pathology | Cells, Cultured | Cerebral Cortex - pathology | Male | Protein Deglycase DJ-1 - genetics | Brain Injuries - genetics | Brain Injuries - metabolism | Parkinson Disease - genetics | Cerebral Cortex - metabolism | Mice, Knockout | Gliosis - pathology | Animals | Mice | Parkinson Disease - metabolism | Protein Stability | Brain Injuries - pathology | SOX9 Transcription Factor - genetics | Organ Culture Techniques | Astrocytes - metabolism | Protein Deglycase DJ-1 - deficiency | Ubiquitin | Tyrosine | Brain | Neurons | Genes | Genetic research | Brain damage | Diagnostic imaging | Hydroxylases | Injuries | Neuroimaging | Traumatic brain injury | Sox9 protein | Parkinsons disease | Tyrosine 3-monooxygenase | Neuronal-glial interactions | Defects | Ubiquitination | Head injuries | Neurodegeneration | Rodents | Neostriatum | Repair | Damage accumulation | Movement disorders | Neurodegenerative diseases | Axonogenesis | Astrocytes | Hydroxylase | Maintenance | PARK7 protein | Gliosis | Brain-derived neurotrophic factor | Magnetic resonance imaging | Destabilization | Brain injury
Sox9 | Parkinson's disease | astrogliosis | brain repair | DJ‐1 | DJ-1 | SYSTEM | PROTEIN | SPINAL-CORD | NEUROSCIENCES | DEGENERATION | PINK1 | GDNF | ROLES | NEURONS | REACTIVE ASTROCYTES | EXPRESSION | SOX9 Transcription Factor - metabolism | Gliosis - genetics | Gliosis - metabolism | Mice, Inbred C57BL | Astrocytes - pathology | Cells, Cultured | Cerebral Cortex - pathology | Male | Protein Deglycase DJ-1 - genetics | Brain Injuries - genetics | Brain Injuries - metabolism | Parkinson Disease - genetics | Cerebral Cortex - metabolism | Mice, Knockout | Gliosis - pathology | Animals | Mice | Parkinson Disease - metabolism | Protein Stability | Brain Injuries - pathology | SOX9 Transcription Factor - genetics | Organ Culture Techniques | Astrocytes - metabolism | Protein Deglycase DJ-1 - deficiency | Ubiquitin | Tyrosine | Brain | Neurons | Genes | Genetic research | Brain damage | Diagnostic imaging | Hydroxylases | Injuries | Neuroimaging | Traumatic brain injury | Sox9 protein | Parkinsons disease | Tyrosine 3-monooxygenase | Neuronal-glial interactions | Defects | Ubiquitination | Head injuries | Neurodegeneration | Rodents | Neostriatum | Repair | Damage accumulation | Movement disorders | Neurodegenerative diseases | Axonogenesis | Astrocytes | Hydroxylase | Maintenance | PARK7 protein | Gliosis | Brain-derived neurotrophic factor | Magnetic resonance imaging | Destabilization | Brain injury
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Loading RightsCell Reports, ISSN 2211-1247, 01/2018, Volume 22, Issue 1, pp. 136 - 148
Recent evidence of prion-like propagation of α-synuclein (α-syn) into neighboring neurons set up a paradigm to elucidate the mechanism of progression of...
SHP-2 | cell-to-cell transmission | SHP-1 | FcγRIIB | α-synuclein | PROTEOLYTIC CLEAVAGE | BETA RECEPTORS | NEGATIVE REGULATION | ALZHEIMERS-DISEASE | NEURODEGENERATION | PATHOLOGY | MODEL | FC-GAMMA-RIIB | GENOME-WIDE ASSOCIATION | PARKINSONS-DISEASE | CELL BIOLOGY
SHP-2 | cell-to-cell transmission | SHP-1 | FcγRIIB | α-synuclein | PROTEOLYTIC CLEAVAGE | BETA RECEPTORS | NEGATIVE REGULATION | ALZHEIMERS-DISEASE | NEURODEGENERATION | PATHOLOGY | MODEL | FC-GAMMA-RIIB | GENOME-WIDE ASSOCIATION | PARKINSONS-DISEASE | CELL BIOLOGY
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Loading RightsExperimental and Molecular Medicine, ISSN 1226-3613, 12/2010, Volume 42, Issue 12, pp. 823 - 832
It has been suggested that brain inflammation is important in aggravation of brain damage and/or that inflammation causes neurodegenerative diseases including...
brain inflammation | neuronal damage | Systemic Inflammation | Brain inflammation | Neuronal damage | Systemic inflammation | MEDICINE, RESEARCH & EXPERIMENTAL | MICROGLIAL ACTIVATION | PARKIN-DEFICIENT MICE | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CEREBROSPINAL-FLUID | systemic inflammation | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | ENDOTHELIAL-CELLS | IN-VIVO | CHRONIC NEURODEGENERATION | NITRIC-OXIDE | GROWTH-FACTOR | Injections, Intravenous | Substantia Nigra - pathology | Astrocytes - pathology | Encephalitis - pathology | Rats | Substantia Nigra - immunology | Encephalitis - immunology | Male | Neutrophil Infiltration | Rats, Sprague-Dawley | Animals | Cell Death | Lipopolysaccharides - pharmacology | Microglia - pathology | Encephalitis - chemically induced | Original | 생화학
brain inflammation | neuronal damage | Systemic Inflammation | Brain inflammation | Neuronal damage | Systemic inflammation | MEDICINE, RESEARCH & EXPERIMENTAL | MICROGLIAL ACTIVATION | PARKIN-DEFICIENT MICE | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CEREBROSPINAL-FLUID | systemic inflammation | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | ENDOTHELIAL-CELLS | IN-VIVO | CHRONIC NEURODEGENERATION | NITRIC-OXIDE | GROWTH-FACTOR | Injections, Intravenous | Substantia Nigra - pathology | Astrocytes - pathology | Encephalitis - pathology | Rats | Substantia Nigra - immunology | Encephalitis - immunology | Male | Neutrophil Infiltration | Rats, Sprague-Dawley | Animals | Cell Death | Lipopolysaccharides - pharmacology | Microglia - pathology | Encephalitis - chemically induced | Original | 생화학
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Loading RightsGlia, ISSN 0894-1491, 05/2013, Volume 61, Issue 5, pp. 800 - 812
PINK1 (PTEN induced putative kinase 1), a familial Parkinson's disease (PD)‐related gene, is expressed in astrocytes, but little is known about its role in...
PINK1 | Parkinson's disease | proliferation | astrocyte | Astrocyte | Proliferation | DJ-1 KNOCK-DOWN | PROTEIN-KINASE | RECEPTOR | NEUROSCIENCES | EPIDERMAL-GROWTH-FACTOR | REACTIVE ASTROCYTES | SPINAL-CORD-INJURY | ABSENCE | EXPRESSION | BRAIN | PARKINSONS-DISEASE | Cell Proliferation | Mice, Inbred C57BL | Astrocytes - pathology | Cells, Cultured | p38 Mitogen-Activated Protein Kinases - biosynthesis | Up-Regulation - genetics | Mitochondria - metabolism | Mice, 129 Strain | Down-Regulation - genetics | Mice, Knockout | Receptor, Epidermal Growth Factor - metabolism | Animals | Mitochondria - genetics | Cattle | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Mice | Protein Kinases - deficiency | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Astrocytes - metabolism | Glucose metabolism | Epidermal growth factor | Glucose | Dextrose | Proteins | Wound healing | Cells | Original s
PINK1 | Parkinson's disease | proliferation | astrocyte | Astrocyte | Proliferation | DJ-1 KNOCK-DOWN | PROTEIN-KINASE | RECEPTOR | NEUROSCIENCES | EPIDERMAL-GROWTH-FACTOR | REACTIVE ASTROCYTES | SPINAL-CORD-INJURY | ABSENCE | EXPRESSION | BRAIN | PARKINSONS-DISEASE | Cell Proliferation | Mice, Inbred C57BL | Astrocytes - pathology | Cells, Cultured | p38 Mitogen-Activated Protein Kinases - biosynthesis | Up-Regulation - genetics | Mitochondria - metabolism | Mice, 129 Strain | Down-Regulation - genetics | Mice, Knockout | Receptor, Epidermal Growth Factor - metabolism | Animals | Mitochondria - genetics | Cattle | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Mice | Protein Kinases - deficiency | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Astrocytes - metabolism | Glucose metabolism | Epidermal growth factor | Glucose | Dextrose | Proteins | Wound healing | Cells | Original s
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Loading RightsJournal of Neuroinflammation, ISSN 1742-2094, 05/2012, Volume 9, Issue 1, pp. 100 - 100
Background: Traumatic spinal cord injury (SCI) causes acute neuronal death followed by delayed secondary neuronal damage. However, little is known about how...
Secondary injury | Monocytes | Spinal cord injury | Astrocytes | Microglia | NEUROTROPHIC FACTOR | MICROGLIAL CELLS | IMMUNOLOGY | NEUROSCIENCES | GLUTAMATE TRANSPORTERS | INFLAMMATORY CELLS | AMINO-ACIDS | MOUSE MODEL | NITRIC-OXIDE | CULTURED ASTROCYTES | RAT-BRAIN | HUNTINGTONS-DISEASE | Neurons - pathology | Calcium-Binding Proteins - biosynthesis | Spinal Cord Injuries - metabolism | Astrocytes - pathology | Contusions - metabolism | Rats | Rats, Sprague-Dawley | Disease Progression | Nerve Degeneration - metabolism | Nerve Degeneration - pathology | Spinal Cord Injuries - pathology | Microfilament Proteins - biosynthesis | Animals | Time Factors | Contusions - pathology | Female | Neurons - metabolism | Astrocytes - metabolism | RNA | Neurons | Analysis | Nervous system | Spinal cord injuries | Degeneration | Glutamate | Proteins | Medical research | Postoperative period | Rodents
Secondary injury | Monocytes | Spinal cord injury | Astrocytes | Microglia | NEUROTROPHIC FACTOR | MICROGLIAL CELLS | IMMUNOLOGY | NEUROSCIENCES | GLUTAMATE TRANSPORTERS | INFLAMMATORY CELLS | AMINO-ACIDS | MOUSE MODEL | NITRIC-OXIDE | CULTURED ASTROCYTES | RAT-BRAIN | HUNTINGTONS-DISEASE | Neurons - pathology | Calcium-Binding Proteins - biosynthesis | Spinal Cord Injuries - metabolism | Astrocytes - pathology | Contusions - metabolism | Rats | Rats, Sprague-Dawley | Disease Progression | Nerve Degeneration - metabolism | Nerve Degeneration - pathology | Spinal Cord Injuries - pathology | Microfilament Proteins - biosynthesis | Animals | Time Factors | Contusions - pathology | Female | Neurons - metabolism | Astrocytes - metabolism | RNA | Neurons | Analysis | Nervous system | Spinal cord injuries | Degeneration | Glutamate | Proteins | Medical research | Postoperative period | Rodents
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Loading RightsScientific Reports, ISSN 2045-2322, 06/2016, Volume 6, Issue 1, p. 28823
Parkinson's disease (PD) is a common chronic and progressive neurodegenerative disorder. Although the cause of PD is still poorly understood, mutations in many...
LOCALIZATION | TRANSPORTERS | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | LIPID RAFTS | AXON REGENERATION | DOWN-REGULATION | ALPHA-SYNUCLEIN | RAT-BRAIN | PROTEINS | PARKINSONS-DISEASE | Membrane Microdomains | Gene Expression Regulation | Homeostasis | Protein Deglycase DJ-1 - genetics | Cholesterol - metabolism | Excitatory Amino Acid Transporter 2 - metabolism | Mice, Knockout | Caveolin 1 - metabolism | Endocytosis | Animals | Central Nervous System | Brain - pathology | Protein Binding | Glutamic Acid - pharmacokinetics | Glutamic Acid - metabolism | Membrane Proteins - metabolism | Mice | Mutation | Astrocytes - metabolism | Protein Deglycase DJ-1 - deficiency
LOCALIZATION | TRANSPORTERS | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | LIPID RAFTS | AXON REGENERATION | DOWN-REGULATION | ALPHA-SYNUCLEIN | RAT-BRAIN | PROTEINS | PARKINSONS-DISEASE | Membrane Microdomains | Gene Expression Regulation | Homeostasis | Protein Deglycase DJ-1 - genetics | Cholesterol - metabolism | Excitatory Amino Acid Transporter 2 - metabolism | Mice, Knockout | Caveolin 1 - metabolism | Endocytosis | Animals | Central Nervous System | Brain - pathology | Protein Binding | Glutamic Acid - pharmacokinetics | Glutamic Acid - metabolism | Membrane Proteins - metabolism | Mice | Mutation | Astrocytes - metabolism | Protein Deglycase DJ-1 - deficiency
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Loading RightsActa Neuropathologica Communications, ISSN 2051-5960, 12/2019, Volume 7, Issue 1
Accumulating evidence indicates that endoplasmic reticulum (ER) stress is a common feature of Parkinson’s disease (PD) and further suggests that several...
Mitochondria | Neurodegeneration | Neurons | Protein folding | Parkinsons disease | Homeostasis | Mutation | Gene expression | Kinases | Endoplasmic reticulum | Autophagy | Apoptosis
Mitochondria | Neurodegeneration | Neurons | Protein folding | Parkinsons disease | Homeostasis | Mutation | Gene expression | Kinases | Endoplasmic reticulum | Autophagy | Apoptosis
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