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Molecular Systems Biology, ISSN 1744-4292, 01/2017, Volume 13, Issue 1, pp. 905 - n/a
Treatment of BRAF‐mutant melanomas with MAP kinase pathway inhibitors is paradigmatic of the promise of precision cancer therapy but also highlights problems with drug resistance that limit patient benefit. We use live... 
adaptive and reversible drug resistance | RAF and MEK inhibitors | BRAFV600E melanomas | de‐differentiated NGFRHigh state | melanomas | BRAF | de-differentiated NGFR | state | CANCER-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACQUIRED-RESISTANCE | SENSITIVITY | de-differentiated NGFR(High) state | RECEPTOR | CONFERS RESISTANCE | BRAF INHIBITION | BRAF(V600E) melanomas | EVOLUTION | PATHWAY | DYNAMICS | REVEALS | Cell Survival - drug effects | Humans | Gene Expression Profiling - methods | Sulfonamides - pharmacology | Nerve Tissue Proteins - genetics | Indoles - administration & dosage | Receptors, Nerve Growth Factor - genetics | Xenograft Model Antitumor Assays | Vemurafenib | Animals | MAP Kinase Signaling System - drug effects | Cell Differentiation - drug effects | Melanoma - genetics | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Indoles - pharmacology | Cell Proliferation - drug effects | Mice | Gene Expression Regulation, Neoplastic - drug effects | Mutation | Single-Cell Analysis | Sulfonamides - administration & dosage | Drug Resistance, Neoplasm - drug effects | Pharmacology | Microbiology | Kinases | Drug resistance | Cancer therapies | Melanoma | Drugs | Biotechnology | Profiling | Transcription | Xenotransplantation | Raf protein | Drug delivery | Experiments | Cell cycle | Xenografts | Extracellular matrix | Drug dosages | Growth factors | Phenotypes | Statistical analysis | Tumor cells | MEK inhibitors | Cloning | Medical school libraries | MAP kinase | MEK kinase | Gene expression | Neural crest | Variance analysis | Inhibitors | Nerve growth factor receptors | Tumors | Apoptosis
Journal Article
Molecular neurobiology, ISSN 1559-1182, 2015, Volume 53, Issue 7, pp. 4286 - 4301
.... Currently, no information is available about the putative mechanism and neuroprotective effects of ALCAR in 6-hydroxydopamine (6-OHDA... 
Neurology | Oxidative stress | Neuroprotection | Neurosciences | Biomedicine | Neuroblasts | Neurobiology | Acetyl- l -carnitine (ALCAR) | Neural stem cells | Wnt/ β -catenin pathway | Cell Biology | Acetyl-l-carnitine (ALCAR) | Wnt/β-catenin pathway | ACETYL-L-CARNITINE | Wnt/beta-catenin pathway | ALPHA-LIPOIC ACID | DOPAMINERGIC-NEURONS | SUBVENTRICULAR ZONE | SUBSTANTIA-NIGRA | NEUROSCIENCES | MGLU2 RECEPTORS | NEURAL STEM-CELLS | MOUSE MODEL | Acetyl-L-carnitine (ALCAR) | HIPPOCAMPAL NEUROGENESIS | CORPUS STRIATUM | Neuroprotective Agents - therapeutic use | Reactive Oxygen Species - metabolism | Acetylcarnitine - pharmacology | Dopaminergic Neurons - pathology | Neuroglia - pathology | Antioxidants - metabolism | Nitrites - metabolism | Male | Parkinson Disease - drug therapy | Oxidopamine | Neuroglia - drug effects | Behavior, Animal | Brain - metabolism | Cell Nucleus - metabolism | Neuroprotective Agents - pharmacology | Dopaminergic Neurons - metabolism | Lipid Peroxidation - drug effects | Ataxia - drug therapy | Dopaminergic Neurons - drug effects | Neurogenesis - drug effects | Parkinson Disease - metabolism | Phosphorylation - drug effects | Disease Models, Animal | Parkinson Disease - complications | Parkinson Disease - pathology | Neural Stem Cells - drug effects | Axons - drug effects | Axons - metabolism | Glycogen Synthase Kinase 3 beta - metabolism | Rats, Sprague-Dawley | Brain - drug effects | Phenotype | Animals | Wnt Signaling Pathway - drug effects | Axons - pathology | Brain - pathology | Neuroglia - metabolism | Ataxia - complications | Acetylcarnitine - therapeutic use | Oxidative Stress - drug effects | Cell Nucleus - drug effects | Neural Stem Cells - metabolism
Journal Article
Cell Reports, ISSN 2211-1247, 02/2018, Volume 22, Issue 8, pp. 2066 - 2079
Journal Article
Journal Article
Nature Neuroscience, ISSN 1097-6256, 08/2013, Volume 16, Issue 8, pp. 1111 - 1117
Relapse to alcohol abuse is an important clinical issue that is frequently caused by cue-induced drug craving... 
AMYGDALA CENTRAL NUCLEUS | MAMMALIAN TARGET | HIPPOCAMPUS | RAPAMYCIN SIGNALING PATHWAY | FEAR MEMORY | NMDA RECEPTORS | RECONSOLIDATION | PLACE PREFERENCE | SYNAPTIC PLASTICITY | NEUROSCIENCES | TRANSLATIONAL CONTROL | Memory - drug effects | Amygdala - physiopathology | Amygdala - drug effects | Binge Drinking - prevention & control | Prefrontal Cortex - physiopathology | Rats, Long-Evans | Protein Biosynthesis - physiology | Conditioning, Operant - physiology | Male | Odorants | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | TOR Serine-Threonine Kinases - antagonists & inhibitors | Ethanol - blood | Prefrontal Cortex - drug effects | Protein Processing, Post-Translational - drug effects | Nerve Tissue Proteins - biosynthesis | Spatial Behavior - drug effects | TOR Serine-Threonine Kinases - physiology | Phosphorylation - drug effects | Cues | Sirolimus - therapeutic use | Rats | Spatial Behavior - physiology | Binge Drinking - psychology | Nerve Tissue Proteins - genetics | Sirolimus - pharmacology | Multiprotein Complexes - physiology | Ethanol - pharmacology | Animals | Signal Transduction - drug effects | Ethanol - chemistry | Neuronal Plasticity | Anisomycin - pharmacology | Protein Biosynthesis - drug effects | Signal Transduction - physiology | Taste | Anisomycin - therapeutic use | Memory - physiology | Psychological aspects | Prevention | Care and treatment | Relapse | Neuropsychiatry | Alcoholism | Memory | Rapamycin | Research | Health aspects | Diseases | memory | Ethanol | relapse | addiction | mTOR | reconsolidation | rapamycin
Journal Article
Cancer cell, ISSN 1535-6108, 2016, Volume 29, Issue 6, pp. 859 - 873
Journal Article
Molecular neurobiology, ISSN 1559-1182, 2018, Volume 55, Issue 9, pp. 7132 - 7152
...Glia Maturation Factor Dependent Inhibition of Mitochondrial PGC-1α Triggers Oxidative Stress-Mediated Apoptosis in N27 Rat Dopaminergic Neuronal Cells... 
Neurology | Oxidative stress | Neurosciences | Biomedicine | Mitochondrial | Neurodegeneration | Neurobiology | Dysfunctions | Parkinson’s disease | Cell Biology | Apoptosis | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | NEURODEGENERATIVE DISORDERS | ACTIVATION | Parkinson's disease | FACTOR-BETA | PROTEIN | DEATH | NEUROBLASTOMA-CELLS | NEUROSCIENCES | PARKINSONS-DISEASE EVIDENCE | DYSFUNCTION | SUPEROXIDE-DISMUTASE | Chromatin - metabolism | Tyrosine 3-Monooxygenase - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Dopaminergic Neurons - pathology | Humans | Cytosol - drug effects | Glia Maturation Factor - pharmacology | Membrane Potential, Mitochondrial - drug effects | Mitochondria - ultrastructure | Oxidative Phosphorylation - drug effects | Caspases - metabolism | Adenosine Triphosphate - metabolism | Dopaminergic Neurons - metabolism | Dopaminergic Neurons - drug effects | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism | Chromatin - ultrastructure | Cell Line | Cell Survival - drug effects | Cytochromes c - metabolism | bcl-2-Associated X Protein - metabolism | Rats | Mitochondria - metabolism | Mitochondria - drug effects | Enzyme Activation - drug effects | Animals | Models, Biological | Cytosol - metabolism | Cell Proliferation - drug effects | Oxidative Stress - drug effects | Cytochrome | Energy metabolism | Bax protein | Bcl-2 protein | Transcription | Pathogenesis | Glia maturation factor | Autophagy | Neuronal-glial interactions | Risk factors | Antioxidants | Depolarization | Mitochondria | Rodents | Membrane potential | Movement disorders | Dopamine receptors | Neurodegenerative diseases | Incubation | Hydroxylase | Caspase | Inflammation | Metabolism | Electron microscopy | Cytochrome c | Transmission electron microscopy | Oxidative phosphorylation | Cell death | Phagocytosis | neurodegeneration | mitochondrial | dysfunctions | oxidative stress
Journal Article
Brain (London, England : 1878), ISSN 1460-2156, 2016, Volume 139, Issue 7, pp. 2063 - 2081
Journal Article