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Clinical Cancer Research, ISSN 1078-0432, 04/2012, Volume 18, Issue 8, pp. 2316 - 2325
Purpose: This study evaluated the clinical relevance of the dual-targeting strategy involving PI3K/AKT/mTOR and RAF/MEK/ERK pathways. Experimental Design: We... 
COLON-CANCER | METASTATIC MELANOMA | PIK3CA MUTATIONS | PI3K | ONCOLOGY | COLORECTAL-CANCER | RESISTANCE | BRAF | ANTITUMOR-ACTIVITY | MEK INHIBITORS | TUMORS | Neoplasms - metabolism | Extracellular Signal-Regulated MAP Kinases - drug effects | TOR Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Middle Aged | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Male | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | TOR Serine-Threonine Kinases - antagonists & inhibitors | Young Adult | MAP Kinase Signaling System - genetics | TOR Serine-Threonine Kinases - genetics | Neoplasms - genetics | Aged, 80 and over | Adult | Female | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | MAP Kinase Signaling System - drug effects | Proto-Oncogene Proteins B-raf - genetics | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Adolescent | Aged | Mutation | Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Journal Article
Journal Article
Nature Neuroscience, ISSN 1097-6256, 08/2017, Volume 20, Issue 8, pp. 1074 - 1084
Aberrant epidermal growth factor receptor (EGFR) signaling is widespread in cancer, making the EGFR an important target for therapy. EGFR gene amplification... 
CANCER-CELLS | GROWTH-FACTOR RECEPTOR | LUNG-CANCER | PHASE-II TRIAL | TARGETED THERAPIES | FEEDBACK ACTIVATION | NEWLY-DIAGNOSED GLIOBLASTOMA | RECURRENT GLIOBLASTOMA | KINASE INHIBITORS | TYROSINE KINASES | NEUROSCIENCES | Cell Survival - drug effects | ErbB Receptors - antagonists & inhibitors | ErbB Receptors - metabolism | Extracellular Signal-Regulated MAP Kinases - drug effects | Humans | ErbB Receptors - genetics | JNK Mitogen-Activated Protein Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Brain Neoplasms - drug therapy | Brain Neoplasms - metabolism | Signal Transduction - drug effects | Cell Line, Tumor | Glioblastoma - metabolism | Antineoplastic Agents - pharmacology | Cell Proliferation - drug effects | Glioblastoma - drug therapy | Epidermal growth factor | Tumor necrosis factor | Extracellular signal-regulated kinases | Cellular signal transduction | Genetic aspects | Research | Gene expression | Glioblastoma multiforme | Tyrosine | Therapy | Transcription factors | Cell survival | Epidermal growth factor receptors | Secretion | Brain tumors | Glioblastoma | c-Jun protein | Extracellular signal-regulated kinase | Kinases | Axl protein | Gene amplification | Glioma cells | Protein-tyrosine kinase receptors | Tumor necrosis factor-TNF | Inhibition | Aberration | Protein-tyrosine kinase | Cancer
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 12/2008, Volume 28, Issue 49, pp. 13248 - 13257
Cue-induced drug-seeking in rodents progressively increases after withdrawal from operant self-administration of cocaine, heroin, methamphetamine, and alcohol,... 
Relapse | CREB | Amygdala | Conditioned place preference | Incubation | Morphine | ERK | amygdala | ACTIVATED PROTEIN-KINASE | INDUCED REINSTATEMENT | conditioned place preference | relapse | INDUCED COCAINE SEEKING | STRESS-INDUCED RELAPSE | ELEMENT-BINDING PROTEIN | NEUROSCIENCES | morphine | VENTRAL TEGMENTAL AREA | NUCLEUS-ACCUMBENS | REINFORCING PROPERTIES | TIME-DEPENDENT CHANGES | incubation | Amygdala - physiopathology | Recurrence | Amygdala - drug effects | MAP Kinase Signaling System - physiology | Extracellular Signal-Regulated MAP Kinases - drug effects | Nitriles - pharmacology | Analgesics, Opioid - pharmacology | Male | Extracellular Signal-Regulated MAP Kinases - metabolism | Cyclic AMP Response Element-Binding Protein - drug effects | Dose-Response Relationship, Drug | Amygdala - enzymology | Time Factors | Phosphorylation - drug effects | Cues | Opioid-Related Disorders - enzymology | Butadienes - pharmacology | Morphine - pharmacology | Conditioning (Psychology) - drug effects | Conditioning (Psychology) - physiology | Enzyme Inhibitors - pharmacology | Rats | Excitatory Amino Acid Agonists - pharmacology | Rats, Sprague-Dawley | Animals | MAP Kinase Signaling System - drug effects | Cyclic AMP Response Element-Binding Protein - metabolism | Environment | Opioid-Related Disorders - physiopathology | Index Medicus
Journal Article
Anesthesiology, ISSN 0003-3022, 04/2016, Volume 124, Issue 4, pp. 934 - 944
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 09/2006, Volume 26, Issue 37, pp. 9439 - 9447
17 beta-Estradiol (E-2)-induced neuroprotection is dependent on mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K) signaling... 
Estrogen receptor | Estrogen signaling | PI3K | Therapeutic development | Akt | Estrogen therapy | MAPK | Alzheimer's disease | estrogen therapy | MEDIATED NEUROPROTECTION | estrogen receptor | AktD | MEDROXYPROGESTERONE ACETATE | estrogen signaling | POTENTIAL INITIATION MECHANISM | PHOSPHOINOSITIDE 3-KINASE | HIPPOCAMPAL-NEURONS | NEUROSCIENCES | therapeutic development | CALCIUM-CHANNELS | SEXUAL-DIFFERENTIATION | ENDOTHELIAL-CELLS | CENTRAL-NERVOUS-SYSTEM | GROWTH-FACTOR-I | Estrogen Replacement Therapy | Protein Subunits - drug effects | MAP Kinase Signaling System - physiology | Receptors, Estrogen - metabolism | Estrogens - pharmacology | Extracellular Signal-Regulated MAP Kinases - drug effects | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Neuroprotective Agents - metabolism | Protein Subunits - metabolism | Neuroprotective Agents - pharmacology | Alzheimer Disease - prevention & control | Phosphatidylinositol 3-Kinases - drug effects | Cerebral Cortex - drug effects | Phosphorylation - drug effects | Estrogens - metabolism | Neurons - drug effects | Oncogene Protein v-akt - metabolism | Estradiol - pharmacology | Estradiol - metabolism | Alzheimer Disease - physiopathology | Cerebral Cortex - enzymology | Receptors, Estrogen - agonists | Oncogene Protein v-akt - drug effects | Cells, Cultured | Rats | Enzyme Activation - drug effects | Rats, Sprague-Dawley | Animals | MAP Kinase Signaling System - drug effects | Neurons - enzymology | Enzyme Activation - physiology
Journal Article
Oncogene, ISSN 0950-9232, 01/2014, Volume 33, Issue 5, pp. 567 - 577
Tumor cells require increased adenosine triphosphate (ATP) to support anabolism and proliferation. The precise mechanisms regulating this process in tumor... 
pancreatic cancer | HMGB1 | RAGE | inflammation | ATP | mitochondria | MIGRATION | SIGNAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | RECEPTOR | AUTOPHAGY | RELEASE | CANCER | GROUP BOX-1 PROTEIN | CELL BIOLOGY | IMMUNE | ONCOLOGY | ADVANCED GLYCATION ENDPRODUCTS | GENETICS & HEREDITY | RNA, Small Interfering - genetics | Cell Proliferation | Extracellular Signal-Regulated MAP Kinases - drug effects | Pancreatic Neoplasms - metabolism | Toll-Like Receptor 2 - genetics | Uncoupling Agents | Nitriles - pharmacology | Humans | Tumor Microenvironment | NF-kappa B - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Adenosine Triphosphate - biosynthesis | Electron Transport Complex I - metabolism | Inflammation - metabolism | RNA Interference | Adenosine Triphosphate - metabolism | HMGB1 Protein - metabolism | Protein Binding - drug effects | Rotenone - pharmacology | CD24 Antigen - genetics | Phosphorylation - drug effects | Protein Synthesis Inhibitors - pharmacology | Receptor for Advanced Glycation End Products - genetics | MAP Kinase Kinase 2 - genetics | Butadienes - pharmacology | Electron Transport Complex I - antagonists & inhibitors | Signal Transduction | Pancreatic Neoplasms - pathology | Receptor for Advanced Glycation End Products - metabolism | Enzyme Inhibitors - pharmacology | Toll-Like Receptor 4 - genetics | HMGB1 Protein - drug effects | MAP Kinase Kinase 2 - metabolism | Mitochondria - metabolism | Mitochondria - drug effects | Cycloheximide - pharmacology | Animals | Energy Metabolism | Cell Line, Tumor | Mice | Cell Movement | NF-kappa B - drug effects | Growth | Oncology, Experimental | Development and progression | Inflammation | Research | Muscle proteins | Necrosis | Mitochondria | Pancreatic cancer | Cancer cells | Physiological aspects | Adenosine triphosphate | Cancer | Studies | Angiogenesis | Adenosine triphosphatase
Journal Article
Neurochemical Research, ISSN 0364-3190, 2/2019, Volume 44, Issue 2, pp. 347 - 356
Hypoxic-ischemic brain injury (HIBI) in neonates is one of the major contributors of newborn death and cognitive impairment. Numerous animal studies have... 
Neurochemistry | Biochemistry, general | Sevoflurane postconditioning (SPC) | Neurology | Neuroprotection | Neurosciences | Biomedicine | Cognitive and memory impairment | Hypoxic-ischemic brain injury (HIBI) | ERK cascade | Autophagy | Cell Biology | APOPTOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MECHANISMS | MODEL | NEUROSCIENCES | DAMAGE | CELL-DEATH | MEMORY | CEREBRAL-ISCHEMIA | LC3 | Memory - drug effects | Extracellular Signal-Regulated MAP Kinases - drug effects | TOR Serine-Threonine Kinases - metabolism | Brain Injuries - drug therapy | Hypoxia-Ischemia, Brain - drug therapy | Rats | Extracellular Signal-Regulated MAP Kinases - metabolism | Autophagy - drug effects | Sevoflurane - pharmacology | Brain - drug effects | Brain - metabolism | Animals | Signal Transduction - drug effects | Ischemic Postconditioning | Proto-Oncogene Proteins c-akt - metabolism | Hypoxia-Ischemia, Brain - metabolism | Sevoflurane | Proteins | Brain | Patient outcomes | Memory | Tuberous sclerosis | Infants | Anesthetics | Injuries | TOR protein | Tuberous sclerosis 2 protein | Neonates | Target recognition | Traumatic brain injury | Spatial discrimination learning | Cognitive ability | Spatial discrimination | Head injuries | Ischemia | Microtubule-associated proteins | Carotid artery | Alveoli | Extracellular signal-regulated kinase | Rapamycin | Latency | Ribosomal protein S6 kinase | TSC2 protein | Inhibitors | Hypoxia | Brain injury | Phagocytosis | Spatial memory
Journal Article
American Journal of Physiology - Endocrinology and Metabolism, ISSN 0193-1849, 08/2016, Volume 311, Issue 2, pp. E530 - E541
To better understand the role of irisin in humans, we examined the effects of irisin in human primary adipocytes and fresh human subcutaneous white adipose... 
Irisin | Thermogenesis | Human white adipose tissue | Brown adipose tissue | Adipocytes browning | Osteogenesis | Adipogenesis | Immunohistochemistry | Thermogenesis - genetics | Up-Regulation | Phosphoproteins - drug effects | Extracellular Signal-Regulated MAP Kinases - drug effects | Adipocytes, Brown - metabolism | Adipogenesis - drug effects | Humans | Middle Aged | Extracellular Signal-Regulated MAP Kinases - metabolism | Phosphoproteins - metabolism | RNA, Messenger - metabolism | Young Adult | Adipocytes, White - drug effects | Exercise | Cell Respiration - drug effects | Adult | Female | p38 Mitogen-Activated Protein Kinases - metabolism | Adipogenesis - genetics | Real-Time Polymerase Chain Reaction | Osteogenesis - genetics | STAT3 Transcription Factor - metabolism | RNA, Messenger - drug effects | Uncoupling Protein 1 - drug effects | Fibronectins - pharmacology | Signal Transduction | Adipocytes, Brown - drug effects | Uncoupling Protein 1 - metabolism | Osteoblasts - drug effects | Osteogenesis - drug effects | Cells, Cultured | Mitochondria - metabolism | Mitochondria - drug effects | Subcutaneous Fat - cytology | Blotting, Western | Obesity - metabolism | p38 Mitogen-Activated Protein Kinases - drug effects | Cell Differentiation - drug effects | STAT3 Transcription Factor - drug effects | Adolescent | Aged | Thermogenesis - drug effects | Osteoblasts - metabolism | Adipocytes, White - metabolism | Fat cells | Growth | Physiological aspects | Bones | Physiological research | Research
Journal Article
Journal of Psychiatric Research, ISSN 0022-3956, 2014, Volume 55, Issue 1, pp. 15 - 21
Journal Article
Annals of Neurology, ISSN 0364-5134, 01/2008, Volume 63, Issue 1, pp. 61 - 71
Objective FTY720, a sphingosine‐1‐phosphate (S1P) receptor agonist that crosses the blood–brain barrier, is a potential immuno‐therapy for multiple sclerosis.... 
SIGNAL-TRANSDUCTION | CELLS | 1-PHOSPHATE RECEPTOR AGONIST | MULTIPLE-SCLEROSIS | LYSOPHOSPHATIDIC ACID | PROCESS RETRACTION | SUBCORTICAL WHITE-MATTER | COUPLED RECEPTORS | G-PROTEIN | NEUROSCIENCES | CLINICAL NEUROLOGY | SPHINGOSINE 1-PHOSPHATE | Lysophospholipids - metabolism | Oligodendroglia - metabolism | Extracellular Signal-Regulated MAP Kinases - drug effects | Receptors, G-Protein-Coupled - metabolism | Humans | Extracellular Signal-Regulated MAP Kinases - metabolism | RNA, Messenger - metabolism | Stem Cells - metabolism | Cell Movement - physiology | rho-Associated Kinases - antagonists & inhibitors | Oligodendroglia - drug effects | rho-Associated Kinases - metabolism | Propylene Glycols - therapeutic use | Receptors, Lysosphingolipid - genetics | Sphingosine - metabolism | Receptors, G-Protein-Coupled - drug effects | Receptors, Lysosphingolipid - metabolism | Cell Differentiation - physiology | Immunosuppressive Agents - pharmacology | Cell Survival - physiology | Suramin - pharmacology | RNA, Messenger - drug effects | Propylene Glycols - pharmacology | Cell Line | Cell Survival - drug effects | Fingolimod Hydrochloride | Down-Regulation - drug effects | Down-Regulation - genetics | Sphingosine - pharmacology | Cell Movement - drug effects | Sphingosine - analogs & derivatives | Signal Transduction - drug effects | Cell Differentiation - drug effects | Cell Surface Extensions - drug effects | Cytoskeleton - metabolism | Receptors, Lysosphingolipid - agonists | Stem Cells - drug effects | Signal Transduction - physiology | Sphingosine - therapeutic use | Cytoskeleton - drug effects
Journal Article