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Journal of Neuroimmunology, ISSN 0165-5728, 2015, Volume 284, pp. 18 - 29
...) and D5R, and how this modulation affects CD4+ T-cell activation and differentiation. Our pharmacologic and genetic evidence shows that D3R-stimulation reduced cAMP levels and ERK2-phosphorylation, consequently increasing CD4... 
Neurology | Allergy and Immunology | Knockout mice | Th1 differentiation | Neuroimmunology | TCR signalling | T-cell activation | Dopamine receptors | IMMUNITY | DENDRITIC CELLS | NEURODEGENERATION | PROLIFERATION | IMMUNOLOGY | NEUROSCIENCES | IN-VITRO | CD4+AND CD8+T CELLS | SECRETION | TH1 | CYTOTOXICITY | LYMPHOCYTES | T-Lymphocytes - physiology | Receptors, Dopamine D3 - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Dose-Response Relationship, Drug | Receptors, Dopamine D3 - genetics | Cell Differentiation - genetics | Lymphocyte Activation - genetics | Phosphorylation - genetics | Dopamine Agents - pharmacology | T-Lymphocytes - drug effects | Phosphorylation - drug effects | Cell Differentiation - physiology | Cyclic AMP - metabolism | Gene Expression Regulation - genetics | Mice, Inbred C57BL | Enzyme Inhibitors - pharmacology | Signal Transduction - genetics | Enzyme Activation - drug effects | Mice, Knockout | Gene Expression Regulation - drug effects | Animals | Interleukin-2 Receptor alpha Subunit - metabolism | Signal Transduction - drug effects | Cell Differentiation - drug effects | Lymphocyte Activation - drug effects | Ionomycin - pharmacology | Receptors, Dopamine D5 - metabolism | Mice | Receptors, Dopamine D5 - genetics | Enzyme Activation - genetics | CD4 Antigens - metabolism
Journal Article
Hypertension, ISSN 0194-911X, 11/2012, Volume 60, Issue 5, pp. 1301 - 1308
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2015, Volume 125, Issue 2, pp. 665 - 680
.... Here, we demonstrated that the mitochondrial uncoupling protein-2 (UCP2) regulates NLRP3-mediated caspase-1 activation through the stimulation of lipid synthesis in macrophages... 
MEDICINE, RESEARCH & EXPERIMENTAL | OXIDATIVE STRESS | GLUCOSE-METABOLISM | ATP-CITRATE LYASE | UCP2 | SEPTIC SHOCK | CELL-GROWTH | CRITICALLY-ILL PATIENTS | INTENSIVE INSULIN THERAPY | CANCER | MITOCHONDRIAL UNCOUPLING PROTEINS | Fatty Acid Synthase, Type I - genetics | Fatty Acid Synthase, Type I - biosynthesis | Lipids - genetics | Inflammasomes - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Ion Channels - genetics | Caspase 1 - metabolism | Mitochondrial Proteins - genetics | Interleukin-1beta - genetics | Lipids - biosynthesis | Sepsis - pathology | Interleukin-1beta - metabolism | Mitochondrial Proteins - metabolism | Sepsis - metabolism | Macrophages - pathology | Down-Regulation - genetics | Inflammasomes - genetics | Sepsis - genetics | Mice, Knockout | Carrier Proteins - genetics | Enzyme Induction - genetics | Macrophages - metabolism | Animals | Carrier Proteins - metabolism | Sepsis - chemically induced | Ion Channels - metabolism | Caspase 1 - genetics | Sepsis - therapy | Mice | Uncoupling Protein 2 | Interleukin-18 - genetics | Interleukin-18 - metabolism | Cellular proteins | Immune response | Synthesis | Sepsis | Development and progression | Lipids | Genetic aspects | Properties | Enzymes | Cytokines | Pathogenesis | Mortality | Glucose | Metabolism | Gene expression | Fatty acids | Proteins | Studies | Metabolites | Consent | Rodents
Journal Article
Nature medicine, ISSN 1546-170X, 2008, Volume 14, Issue 11, pp. 1256 - 1263
Journal Article
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 06/2008, Volume 28, Issue 26, pp. 6652 - 6658
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 07/2016, Volume 36, Issue 29, pp. 7693 - 7706
...) represent an important risk factor for PD, and can lead to alpha-syn accumulation. Here we use a small-molecule modulator of GCase to determine whether GCase activation within lysosomes can reduce alpha-syn levels and ameliorate downstream toxicity... 
Lysosomes | Glucocerebrosidase | Induced pluripotent stem cells | Synucleinopathy | Parkinson’s disease | α-synuclein | synucleinopathy | CELLS | DEFECTS | Parkinson's disease | PARK9 | alpha-synuclein | NEUROSCIENCES | glucocerebrosidase | INHIBITION | ENZYME | MOUSE MODEL | DISEASE | induced pluripotent stem cells | lysosomes | DYSFUNCTION | MUTATIONS | AGGREGATION | Neurodegenerative Diseases - etiology | Humans | Dopaminergic Neurons - ultrastructure | Subcellular Fractions - pathology | Proton-Translocating ATPases - metabolism | Cell Differentiation - genetics | Lysosomes - metabolism | Dopaminergic Neurons - metabolism | Dopaminergic Neurons - drug effects | Neuroblastoma - pathology | Mesencephalon - pathology | Synaptophysin - metabolism | Parkinson Disease - pathology | Neurodegenerative Diseases - pathology | Gene Expression Regulation - genetics | Enzyme Inhibitors - pharmacology | Glucosylceramidase - metabolism | Neurodegenerative Diseases - metabolism | Mutation - genetics | Subcellular Fractions - metabolism | Gene Expression Regulation - drug effects | Cell Differentiation - drug effects | Cell Line, Tumor | Induced Pluripotent Stem Cells | alpha-Synuclein - metabolism | Lysosomal-Associated Membrane Protein 2 - metabolism
Journal Article