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Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2017, Volume 114, Issue 9, pp. 2349 - 2354
.... The understanding of the molecular mechanisms underlying RV replication and pathogenesis has been hampered by the lack of an entirely plasmid-based reverse genetics system... 
SEE COMMENTARY | Vaccine | Reporter virus | Rotavirus | Reverse genetics | reverse genetics | NSP1 | PROTEIN | MULTIDISCIPLINARY SCIENCES | reporter virus | INNATE IMMUNE-RESPONSE | VACCINIA VIRUS | BLUETONGUE VIRUS | CLONED CDNA | vaccine | MESSENGER-RNA | rotavirus | RNA-CAPPING ENZYME | SYNTHETIC RNA | EXPRESSION | Luciferases - metabolism | Cricetulus | Humans | Methyltransferases - metabolism | Reverse Genetics - methods | DNA, Complementary - genetics | Methyltransferases - genetics | Multienzyme Complexes - metabolism | Green Fluorescent Proteins - genetics | Orthoreovirus - metabolism | Vaccinia virus - genetics | Viral Proteins - metabolism | Luciferases - genetics | Base Sequence | Nucleotidyltransferases - metabolism | Genes, Reporter | Cell Line | Green Fluorescent Proteins - metabolism | Phosphoric Monoester Hydrolases - genetics | Transduction, Genetic | Vaccinia virus - metabolism | Orthoreovirus - genetics | Orthoreovirus, Mammalian - genetics | Gene Expression Regulation | Viral Nonstructural Proteins - genetics | Viral Proteins - genetics | DNA-Directed RNA Polymerases - genetics | Multienzyme Complexes - genetics | Plasmids - metabolism | Animals | Epithelial Cells - virology | Plasmids - chemistry | Cell Line, Tumor | Nucleotidyltransferases - genetics | Viral Nonstructural Proteins - metabolism | DNA-Directed RNA Polymerases - metabolism | Phosphoric Monoester Hydrolases - metabolism | DNA, Complementary - metabolism | Orthoreovirus, Mammalian - metabolism | Genetic aspects | Gene expression | Health aspects | Rotaviruses | Biological Sciences
Journal Article
Immunity (Cambridge, Mass.), ISSN 1074-7613, 2012, Volume 37, Issue 2, pp. 249 - 263
Inflammation-mediated neurodegeneration occurs in the acute and the chronic phases of multiple sclerosis (MS) and its animal model, experimental autoimmune... 
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | NITRIC-OXIDE PRODUCTION | INHIBITION | MULTIPLE-SCLEROSIS | PATHWAY | O-GLYCANS | DIFFERENTIATION | IMMUNOLOGY | EXPRESSION | T-CELLS | NEURONAL DYSFUNCTION | Tumor Necrosis Factor-alpha - metabolism | Microglia - metabolism | Central Nervous System - metabolism | Galectin 1 - immunology | Leukocyte Common Antigens - metabolism | Encephalomyelitis, Autoimmune, Experimental - metabolism | Humans | Encephalomyelitis, Autoimmune, Experimental - immunology | Galectin 1 - metabolism | NF-kappa B - metabolism | Central Nervous System - immunology | Multiple Sclerosis - physiopathology | Microglia - immunology | Female | Chemokine CCL2 - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Interleukin-6 - metabolism | Multiple Sclerosis - metabolism | Microglia - cytology | Mice, Inbred C57BL | Mice, Knockout | Polysaccharides - metabolism | Encephalomyelitis, Autoimmune, Experimental - therapy | Animals | Galectin 1 - therapeutic use | Cyclic AMP Response Element-Binding Protein - metabolism | Multiple Sclerosis - immunology | Protein Binding | Mice | Central Nervous System - physiopathology | Astrocytes - metabolism | Nitric Oxide Synthase Type II - metabolism | Multiple sclerosis | Nervous system diseases | Neurosciences | Phosphatases | Analysis | Proteins | Statistical analysis | Neurodegeneration | Rodents | Lectins | Regulation | Kinases | Phosphatase | Immune system | Antigens, CD45 | Astrocytes | Nitric Oxide Synthase Type II | Tumor Necrosis Factor-alpha | Interleukin-6 | Microglia | Multiple Sclerosis | Life Sciences | Encephalomyelitis, Autoimmune, Experimental | Polysaccharides | NF-kappa B | Central Nervous System | Immunology | Chemokine CCL2 | Cyclic AMP Response Element-Binding Protein | p38 Mitogen-Activated Protein Kinases | Galectin 1
Journal Article
The Journal of biological chemistry, ISSN 0021-9258, 06/2014, Volume 289, Issue 24, pp. 16773 - 16789
.... Furthermore, recent studies indicate that LCN2 expression and secretion by glial cells are induced by inflammatory stimuli in the central nervous system... 
PATHOGENESIS | MULTIPLE-SCLEROSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS | NEURON DEATH | REACTIVE ASTROCYTES | CENTRAL-NERVOUS-SYSTEM | GELATINASE-ASSOCIATED LIPOCALIN | CHEMOKINE RECEPTORS | EXPRESSION | CD8(+) T-CELLS | Oncogene Proteins - genetics | Spinal Cord - metabolism | Encephalomyelitis, Autoimmune, Experimental - metabolism | Acute-Phase Proteins - genetics | Interferon-gamma - metabolism | Myelin Sheath - metabolism | Matrix Metalloproteinase 9 - metabolism | T-Lymphocytes - metabolism | Lipocalins - genetics | Matrix Metalloproteinase 9 - genetics | Spinal Cord - pathology | Gene Deletion | Nuclear Receptor Subfamily 1, Group F, Member 3 - metabolism | Interferon-gamma - genetics | Neutrophils - metabolism | Dendritic Cells - metabolism | Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics | Lipocalins - metabolism | Acute-Phase Proteins - metabolism | Mice, Inbred C57BL | Cells, Cultured | Oncogene Proteins - metabolism | Interleukin-17 - genetics | Lymphoid Tissue - metabolism | Receptors, Cell Surface - metabolism | Interleukin-17 - metabolism | Lymphoid Tissue - pathology | Animals | Lipocalin-2 | Myelin Sheath - genetics | Mice | Astrocytes - metabolism | Receptors, Cell Surface - genetics | Multiple Sclerosis | Autoimmune Disease | Central Nervous System | Neurobiology | EAE | LCN2 | Neuroinflammation | Astrocyte | Microglia
Journal Article
Immunity (Cambridge, Mass.), ISSN 1074-7613, 2017, Volume 47, Issue 3, pp. 566 - 581.e9
... period of time. However, apoptosis, as well as neuritic dystrophy leading to permanent central nervous system (CNS) damage, occurs in neurodegenerative diseases... 
Alzheimer’s disease | multiple sclerosis | transcriptional regulation | neurodegeneration | TREM2 | APOE | amyotrophic lateral sclerosis | microglia | Alzheimer's disease | GENE-EXPRESSION SIGNATURE | ACTIVATION | MULTIPLE-SCLEROSIS | ALZHEIMERS-DISEASE | MOUSE MODEL | MACROPHAGE | MICE | IMMUNOLOGY | DEFICIENCY | APOLIPOPROTEIN-E | CELL-DEATH | Microglia - metabolism | Apolipoproteins E - deficiency | Membrane Glycoproteins - metabolism | Humans | Cerebral Cortex - pathology | Transcriptome | Apoptosis - genetics | Monocytes - metabolism | Gene Expression Profiling | Monocytes - immunology | Phagocytosis - genetics | Neurodegenerative Diseases - immunology | Apolipoproteins E - metabolism | Cerebral Cortex - metabolism | Alzheimer Disease - pathology | Microglia - immunology | Superoxide Dismutase-1 - metabolism | Amyloid beta-Peptides - metabolism | Amyloid beta-Protein Precursor - metabolism | Female | Neurons - metabolism | Disease Models, Animal | Gene Targeting | Plaque, Amyloid - pathology | Signal Transduction | Gene Expression Regulation | Phagocytosis - immunology | Immune Tolerance | Mice, Transgenic | Neurodegenerative Diseases - genetics | Neurodegenerative Diseases - metabolism | Mice, Knockout | Encephalomyelitis, Autoimmune, Experimental | Phenotype | Animals | Apoptosis - immunology | Apolipoproteins E - genetics | Alzheimer Disease - metabolism | Superoxide Dismutase-1 - genetics | Plaque, Amyloid - metabolism | Mice | Alzheimer Disease - genetics | Transforming Growth Factor beta - metabolism | Receptors, Immunologic - metabolism | Cluster Analysis | Nervous system diseases | Multiple sclerosis | Neurons | Analysis | Amyotrophic lateral sclerosis | Genetic aspects | Genetic transcription | Apolipoproteins | Brain | Animal models | Myeloid cells | Disease | Transcription | Neurodegenerative diseases | Genes | Homeostasis | Microglia | Neurological diseases | Proteins | Molecular modelling | Restoration | Neurodegeneration | Apolipoprotein E | Rodents | β-Amyloid | Plaques | Phagocytosis | Apoptosis
Journal Article
PloS one, ISSN 1932-6203, 2015, Volume 10, Issue 6, pp. e0130624 - e0130624
Neuroinflammation is the local reaction of the brain to infection, trauma, toxic molecules or protein aggregates. The brain resident macrophages, microglia,... 
INTERLEUKIN-1 | ACTIVATION | MOLECULAR PLATFORM | INHIBITION | DISTINCT PATHWAYS | NEUROINFLAMMATION | MULTIDISCIPLINARY SCIENCES | IL-1-BETA | MECHANISMS | RECEPTORS | NALP3 INFLAMMASOME | Microglia - metabolism | Inflammasomes - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Peptide Fragments - toxicity | Caspase 1 - metabolism | Interleukin-1alpha - metabolism | alpha-Synuclein - pharmacology | Interleukin-1beta - metabolism | Interleukin-1beta - secretion | Microglia - cytology | Brain - cytology | Interleukin-1beta - analysis | Enzyme-Linked Immunosorbent Assay | Microglia - drug effects | Amyloid beta-Peptides - toxicity | Mice, Inbred C57BL | Cells, Cultured | Mice, Knockout | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Caspase 1 - genetics | Caspase 1 - deficiency | Receptors, Purinergic P2X7 - metabolism | Mice | Interleukin-18 - metabolism | Astrocytes - metabolism | Cytokines | Health aspects | Nervous system diseases | Brain | Cell culture | Traumatic brain injury | Peptides | Aluminum sulfate | Homeostasis | Nervous system | Activation | Macrophages | Synuclein | Proteins | Rodents | Amyloid | Life sciences | Communication | Immune system | Neurodegenerative diseases | Astrocytes | Inflammation | Trauma | Molecular chains | Microglia | Interleukin 18 | Mode of action | Neurological diseases | Nigericin | Brain research | Ligands | Alum | Laboratory animals | Alzheimers disease | Chemokines | Index Medicus
Journal Article
Nature (London), ISSN 1476-4687, 2011, Volume 472, Issue 7343, pp. 361 - 365
TRIM5 is a RING domain-E3 ubiquitin ligase that restricts infection by human immunodeficiency virus (HIV)-1 and other retroviruses immediately following virus... 
HIV-1 | CYCLOPHILIN-A | UNANCHORED POLYUBIQUITIN CHAINS | TRIM5-ALPHA PROTEIN | RECOGNITION | HUMAN-CELLS | MULTIDISCIPLINARY SCIENCES | IMMUNODEFICIENCY-VIRUS TYPE-1 | RESISTANCE | INFECTION | RESTRICTION | Capsid - chemistry | Receptors, Pattern Recognition - immunology | Humans | Ubiquitin - metabolism | NF-kappa B - metabolism | Lipopolysaccharides - immunology | Transcription Factor AP-1 - metabolism | Receptors, Pattern Recognition - metabolism | Signal Transduction - immunology | Ubiquitin-Protein Ligases - immunology | HIV-1 - chemistry | HEK293 Cells | Carrier Proteins - immunology | Cell Line | Retroviridae - chemistry | Ubiquitin-Protein Ligases - metabolism | Retroviridae - immunology | MAP Kinase Kinase Kinases - metabolism | Transcription Factors - metabolism | Capsid - immunology | Carrier Proteins - genetics | Immunity, Innate - immunology | HIV-1 - immunology | Carrier Proteins - metabolism | Signal Transduction - drug effects | Ubiquitin-Conjugating Enzymes - metabolism | Lipopolysaccharides - pharmacology | Protein Binding | Enzyme Activation | Ubiquitin-Protein Ligases - genetics | Signal transduction | Efficiency | RNA polymerase | Pattern recognition | Kinases | Evacuations & rescues | Immune system | HIV-1/immunology | Capsid/immunology | Life Sciences | MAP Kinase Kinase Kinases/metabolism | Carrier Proteins/immunology | Immunology | Transcription Factors/metabolism | Capsid/chemistry | HIV-1/chemistry | Ubiquitin/metabolism | Receptors, Pattern Recognition/immunology | Retroviridae/chemistry | Ubiquitin-Protein Ligases/immunology | Ubiquitin-Conjugating Enzymes/metabolism | HumansImmunity, Innate/immunology | Lipopolysaccharides/pharmacology | Signal Transduction/drug effects | Retroviridae/immunology | Transcription Factor AP-1/metabolism | Lipopolysaccharides/immunology | Ubiquitin-Protein Ligases/metabolism | Carrier Proteins/genetics | Signal Transduction/immunology | NF-kappa B/metabolism | Ubiquitin-Protein Ligases/genetics | Carrier Proteins/metabolism | Receptors, Pattern Recognition/metabolism
Journal Article
PloS one, ISSN 1932-6203, 2017, Volume 12, Issue 1, p. e0169648
The structural maintenance of chromosome 5/6 complex (Smc5/6) is a restriction factor that represses hepatitis B virus (HBV) transcription. HBV counters this... 
CELLS | NUCLEAR-BODIES | HEPATITIS-B-VIRUS | REPLICATION | DNA | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | EPIGENETIC REGULATION | COMPONENTS | BINDING | HUMANIZED MICE | Autoantigens - metabolism | Hepatitis B - metabolism | Antigens, Nuclear - metabolism | Humans | Hepatitis B - virology | Male | Hepatocytes - metabolism | Autoantigens - genetics | Hepatitis B - immunology | Hepatocytes - cytology | Trans-Activators - genetics | Cell Cycle Proteins - genetics | Promyelocytic Leukemia Protein - metabolism | Nuclear Proteins - genetics | Cytokines - genetics | Hepatitis B virus - immunology | Promyelocytic Leukemia Protein - genetics | Cytokines - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Chromosomal Proteins, Non-Histone | Nuclear Proteins - metabolism | Mice, SCID | Immunity, Innate - immunology | Animals | Antigens, Nuclear - genetics | Virus Replication | Trans-Activators - metabolism | Mice | Immune response | Analysis | Genetic aspects | Hepatitis B virus | Research | Genetic transcription | Hepatitis B | Cell culture | HBX protein | Pathogenesis | Viruses | Infections | Genomes | Degradation | Proteins | Hepatitis | Hepatology | Localization | Bioinformatics | Chromosomes | Deoxyribonucleic acid--DNA | Immune system | Antigens | Cytokines | Chromosome 5 | Gene expression | Ribonucleic acid--RNA | Hepatocytes | Interferon | Kinetics | RNA | Deoxyribonucleic acid | Ribonucleic acid
Journal Article
Journal Article
PLoS pathogens, ISSN 1553-7374, 2013, Volume 9, Issue 4, p. e1003248
.... In this study, we revealed a novel mechanism in which hepatitis C virus (HCV) evades the immune surveillance system to proliferate by activating microRNA-21 (miR-21... 
RNA REPLICATION | HEPATITIS-C-VIRUS | MICROBIOLOGY | PROTEIN-SYNTHESIS | ALPHA-INTERFERON | I INTERFERON | VIROLOGY | SIGNALING PATHWAY | GENE-EXPRESSION | CYCLOOXYGENASE-2 EXPRESSION | NF-KAPPA-B | DEPENDENT ACTIVATION | PARASITOLOGY | Interleukin-1 Receptor-Associated Kinases - metabolism | RNA Helicases - metabolism | Up-Regulation | Phosphorylation | Interleukin-1 Receptor-Associated Kinases - genetics | Hepacivirus - immunology | Humans | Adaptor Proteins, Vesicular Transport - genetics | Hepacivirus - genetics | Hepacivirus - pathogenicity | JNK Mitogen-Activated Protein Kinases - metabolism | MicroRNAs - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Interferon Regulatory Factor-3 - genetics | MAP Kinase Signaling System | Hepatitis C - immunology | RNA Interference | Protein Kinase C - metabolism | HEK293 Cells | Interferon-alpha - metabolism | Toll-Like Receptor 7 - metabolism | Interferon-alpha - biosynthesis | Myeloid Differentiation Factor 88 - genetics | Proto-Oncogene Proteins c-fos - metabolism | MicroRNAs - immunology | Immune Evasion | Cell Line, Tumor | Viral Nonstructural Proteins - metabolism | MicroRNAs - genetics | RNA, Small Interfering | Serine Endopeptidases - metabolism | Myeloid Differentiation Factor 88 - metabolism | Virus diseases | Immune response | MicroRNA | Cellular control mechanisms | Research | Observations | Hepatitis C virus | Properties | Testing | Proteins | Hepatitis | Kinases | Viral infections | Immune system
Journal Article