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Neurobiology of Disease, ISSN 0969-9961, 12/2018, Volume 120, pp. 76 - 87
Journal Article
British Journal of Pharmacology, ISSN 0007-1188, 09/2008, Volume 155, Issue 1, pp. 73 - 83
Background and purpose: Our previous studies have shown that morphine withdrawal induced hyperactivity of cardiac noradrenergic pathways. The purpose of the... 
noradrenaline turnover | PKA | morphine withdrawal | PKC | TH phosphorylation | heart | ERK | Heart | Morphine withdrawal | Noradrenaline turnover | PROTEIN-KINASE-A | ACTIVATION | ERK SIGNALING PATHWAY | IDENTIFICATION | HYPOTHALAMIC PARAVENTRICULAR NUCLEUS | DEPENDENCE | TYROSINE-HYDROXYLASE PHOSPHORYLATION | PHARMACOLOGY & PHARMACY | INHIBITORS | CONTRIBUTES | C-FOS EXPRESSION | Tyrosine 3-Monooxygenase - metabolism | Phosphorylation | Aminoacetonitrile - analogs & derivatives | Substance Withdrawal Syndrome - etiology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Serine | Drug Implants | Male | Narcotic Antagonists | Isoquinolines - pharmacology | Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors | Naphthalenes - metabolism | Morphine Dependence - enzymology | Disease Models, Animal | Cyclic AMP-Dependent Protein Kinases - metabolism | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Substance Withdrawal Syndrome - enzymology | Rats | Sulfonamides - pharmacology | Rats, Sprague-Dawley | Protein Kinase C-delta - metabolism | Myocardium - enzymology | Animals | Naloxone | Norepinephrine - metabolism | Mitogen-Activated Protein Kinase 3 - metabolism | Protein Kinase Inhibitors - pharmacology | Aminoacetonitrile - pharmacology | Morphine - administration & dosage | Mitogen-Activated Protein Kinase 1 - metabolism | Index Medicus | Research Papers
Journal Article
Behavioural Brain Research, ISSN 0166-4328, 2012, Volume 226, Issue 1, pp. 351 - 356
► Neonatal LPS exposure predisposes to anxiety-like phenotype in adulthood. ► The anxiety-like phenotype is associated with increased hippocampal microglial... 
Postnatal | Anxiety behaviour | TH phosphorylation | HPA axis | LPS | Microglial activation | Hippocampus | PHOSPHORYLATION | ADULTHOOD | LIFE ALTERS | ANXIETY-LIKE BEHAVIOR | NEUROSCIENCES | RESPONSES | ENDOTOXIN EXPOSURE | ANIMAL-MODELS | LIPOPOLYSACCHARIDE | BEHAVIORAL SCIENCES | STRESS | Brain | Animal behavior
Journal Article
Journal Article
BBA - Proteins and Proteomics, ISSN 1570-9639, 2003, Volume 1645, Issue 2, pp. 123 - 132
Tec family protein tyrosine kinases (TFKs) play a central role in hematopoietic cellular signaling. Initial activation takes place through specific tyrosine... 
Tyrosine kinase | Itk | Signal transduction | Tec | Immunodeficiency | Btk | Bmx | X-linked agammaglobulinemia | XLA | signal transduction | BIOCHEMISTRY & MOLECULAR BIOLOGY | tyrosine kinase | TH DOMAIN | x-linked agammaglobulinemia | MICE LACKING | PROLINE-RICH SEQUENCES | REGULATORY DOMAINS | BIOPHYSICS | immunodeficiency | SRC FAMILY | ASSOCIATION | INTERMOLECULAR INTERACTIONS
Journal Article
Metabolism, ISSN 0026-0495, 12/2017, Volume 77, pp. 39 - 46
Metabolic reprogramming is shaped to support specific cell functions since cellular metabolism controls the final outcome of immune response. Multiple... 
Adipocytokines | IFN beta-1a | Multiple sclerosis | Metabolism | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | ACTIVATION | RECEPTOR | OSTEOPROTEGERIN | INTERFERON-BETA | CEREBROSPINAL-FLUID | INFLAMMATION | ENDOCRINOLOGY & METABOLISM | GLATIRAMER ACETATE | LIGAND | Interferon beta-1a - therapeutic use | Multiple Sclerosis, Relapsing-Remitting - immunology | Lymphocyte Activation | Humans | Middle Aged | Oxidative Phosphorylation | Glucose Transporter Type 1 - metabolism | Male | Mitochondria - metabolism | Glycolysis - drug effects | Case-Control Studies | Young Adult | T-Lymphocytes - metabolism | Glucose Transporter Type 1 - drug effects | Adult | Female | T-Lymphocytes - pathology | Multiple Sclerosis, Relapsing-Remitting - metabolism | Glucose metabolism | Enzymes | Relapse | Physiological aspects | Interferon | Biological response modifiers | T cells | Diseases | OCR, oxygen consumption rate | Th, T helper | E2, exone2 | MPO, myeloperoxidase | CIA, collagen-induced arthritis | DLAT, dihydrolipoamide S-acetyltransferase | BMI, body mass index | sICAM-1, soluble ICAM-1 | Tconv, conventional T cells | MCP-1, monocyte chemoattractant protein-1 | PBMCs, peripheral blood mononuclear cells | IFN, interferon | Treg, regulatory T cells | OPG, osteoprotegerin | RANKL, receptor activator of nuclear factor kappaB ligand | T1D, type 1 diabetes | sCD40L, soluble CD40 ligand | RR, relapsing remitting | sTNF-R, soluble tumor necrosis factor receptor | MS, multiple sclerosis | CNS, central nervous system | iTreg, inducible regulatory T cells | ECAR, extracellular acidification rate | sLeptinR, soluble leptin receptor | DLST, dihydrolipoamide succinyltransferase | TCR, T cell receptor | EAE, experimental autoimmune encephalomyelitis
Journal Article
Neurochemistry International, ISSN 0197-0186, 08/2012, Volume 61, Issue 3, pp. 433 - 440
Journal Article
Journal Article
Journal Article
Psychopharmacology, ISSN 0033-3158, 3/2012, Volume 220, Issue 2, pp. 379 - 393
Evidence suggests that corticotropin-releasing factor (CRF) system is an important mediator in the negative symptoms of opioid withdrawal.We used genetically... 
Total TH | Neurosciences | Naloxone-induced withdrawal | Biomedicine | Phospho-Ser40TH | Aversion | Phospho-Ser31TH | Pharmacology/Toxicology | CRF1R-deficient mice | Psychiatry | CONDITIONED PLACE AVERSION | ENDOGENOUS ENKEPHALINS | NOREPINEPHRINE | PSYCHIATRY | CELL GROUP | OPIATE WITHDRAWAL | DRUG-SEEKING | NEUROSCIENCES | HYPOTHALAMIC PARAVENTRICULAR NUCLEUS | CORTICOTROPIN-RELEASING-FACTOR | TYROSINE-HYDROXYLASE PHOSPHORYLATION | PHARMACOLOGY & PHARMACY | NORADRENERGIC NEURONS | Tyrosine 3-Monooxygenase - metabolism | Phosphorylation | Adrenergic Neurons - metabolism | Molecular Imaging - psychology | Receptors, Corticotropin-Releasing Hormone - genetics | Male | Molecular Imaging - methods | Avoidance Learning - physiology | Mice, Inbred Strains | Mice, Knockout | Brain - metabolism | Corticotropin-Releasing Hormone - physiology | Receptors, Corticotropin-Releasing Hormone - physiology | Tyrosine 3-Monooxygenase - biosynthesis | Animals | Substance Withdrawal Syndrome - metabolism | Naloxone - pharmacology | Dopaminergic Neurons - metabolism | Weight Loss - physiology | Mice | Morphine - administration & dosage | Substance Withdrawal Syndrome - psychology | Morphine - adverse effects | Immunohistochemistry | Corticotropin releasing hormone | Brain | Neurons | Analysis | DNA | Genetically modified organisms | ACTH | Accountants | Morphine | Genetic engineering | Drug addiction | Immunology | Rodents | Deoxyribonucleic acid--DNA | Emotional behavior | Opioid receptors | Brain stem | Withdrawal | Data processing | Body weight loss | Corticotropin-releasing hormone | Tails | Polymerase chain reaction | Opioids | Medulla oblongata | c-Fos protein
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 01/2019, Volume 130, pp. 318 - 327
Superoxide generation by mitochondria respiratory complexes is a major source of reactive oxygen species (ROS) which are capable of initiating redox signaling... 
MitoParaquat | Zebrafish | Mitochondria | Superoxide | Parkinson's disease | Huntington's disease | BIOCHEMISTRY & MOLECULAR BIOLOGY | MUTANT HUNTINGTIN | MECHANISMS | MODEL | DISEASES | ROLES | IN-VIVO | ENDOCRINOLOGY & METABOLISM | NEURONS | ASSAYS | MODULATION | Reactive Oxygen Species - metabolism | Humans | Huntington Disease - pathology | Parkinson Disease - drug therapy | Brain - metabolism | Protein Aggregation, Pathological - pathology | Oxidation-Reduction - drug effects | Rotenone - pharmacology | Superoxides - metabolism | Parkinson Disease - metabolism | Huntington Disease - drug therapy | Paraquat - pharmacology | Protein Aggregation, Pathological - genetics | Parkinson Disease - pathology | Mitochondria - metabolism | Antioxidants - pharmacology | Mitochondria - drug effects | Parkinson Disease - genetics | Protein Aggregation, Pathological - drug therapy | Brain - drug effects | Tyrosine 3-Monooxygenase - genetics | Phenotype | Animals | Brain - pathology | Huntington Disease - genetics | Huntingtin Protein - genetics | Oxidative Stress - drug effects | NAC, N-acetyl-L-cysteine | HD, Huntington's disease | Htt, Huntingtin | MitoPQ, MitoParaquat | Dpf, days post fertilization | PBST, phosphate buffer solution with 0.05% Tween 20 | PD, Parkinson's disease | OXPHOS, oxidative phosphorylation | mHtt, mutant huntingtin | TH, tyrosine hydroxylase | ROS, reactive oxygen species
Journal Article