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1. Full Text Fluoxetine-mediated 5-HT2B receptor stimulation in astrocytes causes EGF receptor transactivation and ERK phosphorylation
by Li, Baoman and Zhang, Shiquen and Zhang, Hongyan and Nu, Weiwei and Cai, Liping and Hertz, Leif and Peng, Liang
Psychopharmacology, ISSN 0033-3158, 12/2008, Volume 201, Issue 3, pp. 443 - 458
Fluoxetine has relatively high affinity for Gq/11 protein-coupled 5-HT2 receptors. Part of these receptors in brain are on astrocytes, where fluoxetine causes... 
Neurosciences | Biomedicine | Serotonin | Astrocytes | Fluoxetine | EGFR transactivation | fosB | c-fos | Pharmacology/Toxicology | Psychiatry | ERK | 5-HT 2B receptor | receptor | C-fos | FosB | 5-HT | SIGNALING PATHWAYS | PSYCHIATRY | TYROSINE KINASE | PHARMACOLOGICAL CHARACTERIZATION | CELL-PROLIFERATION | 5-HT2B receptor | NEUROSCIENCES | SEROTONIN REUPTAKE INHIBITORS | MESSENGER-RNA | TISSUE DISTRIBUTION | MECHANICAL-STRESS | CULTURED ASTROCYTES | PHARMACOLOGY & PHARMACY | R-FLUOXETINE | Receptor, Epidermal Growth Factor - genetics | Up-Regulation | Phosphorylation | Transcriptional Activation - genetics | Nitriles - pharmacology | Calcium - metabolism | Maleimides - pharmacology | Substrate Specificity | Extracellular Signal-Regulated MAP Kinases - metabolism | Quinazolines | Calcium - chemistry | Receptor, Serotonin, 5-HT2B - physiology | Dose-Response Relationship, Drug | Fluorobenzenes - pharmacology | Receptor, Epidermal Growth Factor - metabolism | Piperidines - pharmacology | Receptor, Serotonin, 5-HT2B - drug effects | Urea - analogs & derivatives | Egtazic Acid - analogs & derivatives | Indoles - pharmacology | Proto-Oncogene Proteins c-fos - antagonists & inhibitors | Astrocytes - drug effects | Fluoxetine - pharmacology | Butadienes - pharmacology | Gene Expression | Signal Transduction | Dipeptides - pharmacology | RNA, Messenger - genetics | Cells, Cultured | Proto-Oncogene Proteins c-fos - metabolism | Antidepressive Agents, Second-Generation - pharmacology | Protein Kinase C - antagonists & inhibitors | Tyrphostins - pharmacology | Chelating Agents - pharmacology | Antidepressive Agents, Second-Generation - antagonists & inhibitors | Fluoxetine - antagonists & inhibitors | Astrocytes - physiology | Animals | Egtazic Acid - pharmacology | Aminopyridines - pharmacology | Proto-Oncogene Proteins c-fos - genetics | Mice | Urea - pharmacology | Brain | Neurotransmitters | Antidepressants | Psychopharmacology | Cells
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2. Full Text Homocysteine Mediated Expression and Secretion of Monocyte Chemoattractant Protein-1 and Interleukin-8 in Human Monocytes
by Zeng, Xiaokun and Dai, Jing and Remick, Daniel G and Wang, Xian
Circulation Research: Journal of the American Heart Association, ISSN 0009-7330, 08/2003, Volume 93, Issue 4, pp. 311 - 320
ABSTRACT—Homocysteine (Hcy) is an independent risk factor for cardiovascular disease. Monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) are... 
Monocyte chemoattractant protein-1 | Monocytes | Homocysteine | Interleukin-8 | Atherosclerosis | homocysteine | atherosclerosis | monocytes | ENDOTHELIAL-CELL INJURY | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | OXIDANT STRESS | monocyte chemoattractant protein-1 | RISK FACTOR | PLASMA HOMOCYST(E)INE | interleukin-8 | VASCULAR-DISEASE | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | ATHEROMATOUS PLAQUES | HEMATOLOGY | NF-KAPPA-B | T-LYMPHOCYTES | Interleukin-8 - genetics | Reactive Oxygen Species - metabolism | Chemokine CCL2 - secretion | Monocytes - cytology | Humans | Dimethyl Sulfoxide - pharmacology | Monocytes - metabolism | RNA, Messenger - metabolism | Pyrrolidines - pharmacology | Dose-Response Relationship, Drug | Thiocarbamates - pharmacology | Chromans - pharmacology | Time Factors | Homocysteine - pharmacology | Indoles - pharmacology | Interleukin-8 - secretion | Flavonoids - pharmacology | RNA, Messenger - drug effects | RNA, Messenger - genetics | Cells, Cultured | Enzyme Inhibitors - pharmacology | Chemokine CCL2 - genetics | Imidazoles - pharmacology | Tyrphostins - pharmacology | Antioxidants - pharmacology | Onium Compounds - pharmacology | Sulfonamides - pharmacology | Naphthalenes - pharmacology | Gene Expression Regulation - drug effects | Monocytes - drug effects | Genistein - pharmacology | Pyridines - pharmacology | Thiazoles - pharmacology | Thiazolidinediones
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3. Full Text Zinc pyrithione inhibits caspase-3 activity, promotes ErbB1-ErbB2 heterodimerization and suppresses ErbB2 downregulation in cardiomyocytes subjected to ischemia/reperfusion
by Bodiga, Vijaya Lakshmi and Bodiga, Sreedhar and Thokala, Sandhya and Vemuri, Praveen Kumar
Journal of Inorganic Biochemistry, ISSN 0162-0134, 12/2015, Volume 153, pp. 49 - 59
Heart tissue becomes zinc-depleted and the capacity to mobilize labile zinc is diminished, indicating zinc dyshomeostasis during ischemia/reperfusion (I/R).... 
Hypoxia | Reoxygenation | Proteolysis | Caspase-3 | Zinc | Apoptosis | ACTIVATION | RAT | MITOCHONDRIAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | REPERFUSION INJURY | CARDIOMYOPATHY | CARDIAC-CELLS | DEATH | INTRACELLULAR ZINC | CHEMISTRY, INORGANIC & NUCLEAR | ACUTE MYOCARDIAL-INFARCTION | Receptor, Epidermal Growth Factor - genetics | Caspase Inhibitors - pharmacology | Phosphorylation | Receptor, ErbB-2 - genetics | Protein Multimerization | Caspase 3 - metabolism | Receptor, ErbB-2 - metabolism | RNA, Messenger - metabolism | Cell Hypoxia | Receptor, Epidermal Growth Factor - metabolism | Zinc Compounds - pharmacology | Amino Acid Chloromethyl Ketones - pharmacology | Receptor, ErbB-2 - antagonists & inhibitors | Proteasome Inhibitors - pharmacology | Benzothiazoles - pharmacology | Chlorides - pharmacology | Down-Regulation | RNA, Messenger - genetics | Rats | Tyrphostins - pharmacology | Cardiotonic Agents - pharmacology | Leupeptins - pharmacology | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - drug effects | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Thiones - pharmacology | Quinazolines - pharmacology | Organometallic Compounds - pharmacology | Proteins | Membrane lipids | Inositol | RNA | Antifungal agents | Permeability | Antibacterial agents | Phosphotransferases | Tyrosine | Cell death
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4. Full Text LPS-induced autophagy is mediated by oxidative signaling in cardiomyocytes and is associated with cytoprotection
by Hua Yuan and Cynthia N. Perry and Chengqun Huang and Eri Iwai-Kanai and Raquel S. Carreira and Christopher C. Glembotski and Roberta A. Gottlieb
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 02/2009, Volume 296, Issue 2, pp. 470 - 479
Bacterial endotoxin lipopolysaccharide (LPS) is responsible for the multiorgan dysfunction that characterizes septic shock and is causal in the myocardial... 
Green fluorescent protein- Microtubule-associated protein light chain 3 | Lipopolysaccharide | Oxidative stress | Hl-1 cardiac myocyte | TRANSCRIPTIONAL ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | HL-1 cardiac myocyte | CARDIAC MYOCYTES | NECROSIS-FACTOR-ALPHA | MYOCARDIAL DEPRESSION | PROGRAMMED CELL-DEATH | ENDOTOXEMIC RATS | SCAVENGER RECEPTOR | green fluorescent protein-microtubule-associated protein light chain 3 | SEPTIC SHOCK | PERIPHERAL VASCULAR DISEASE | TNF-ALPHA | lipopolysaccharide | NF-KAPPA-B | oxidative stress | Tumor Necrosis Factor-alpha - metabolism | Mitochondria, Heart - metabolism | Glutathione - metabolism | Mitochondria, Heart - pathology | Nitric Oxide Synthase - antagonists & inhibitors | omega-N-Methylarginine - pharmacology | Mitochondria, Heart - drug effects | Nitroprusside - pharmacology | Autophagy - drug effects | p38 Mitogen-Activated Protein Kinases - metabolism | Nitric Oxide Donors - pharmacology | Cytoprotection | Animals, Newborn | Cells, Cultured | Enzyme Inhibitors - pharmacology | Rats | Mice, Transgenic | Imidazoles - pharmacology | Tyrphostins - pharmacology | Antioxidants - pharmacology | Sirolimus - pharmacology | Hydrogen Peroxide - metabolism | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - drug effects | Signal Transduction - drug effects | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Acetylcysteine - pharmacology | Lipopolysaccharides - pharmacology | Myocytes, Cardiac - metabolism | Mice | Nitric Oxide Synthase - metabolism | Pyridines - pharmacology | Oxidative Stress - drug effects | Nitric Oxide - metabolism | Index Medicus
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5. Full Text Targeting Stat3 in cancer therapy
by Jing, Naijie and Tweardy, David J
Anti-Cancer Drugs, ISSN 0959-4973, 07/2005, Volume 16, Issue 6, pp. 601 - 607
Stat3 is constitutively activated in many human cancers where it functions as a critical mediator of oncogenic signaling through transcriptional activation of... 
Stat3 | Cancer therapy | G-quartet oligodeoxynucleotide | COLONY-STIMULATING FACTOR | CONSTITUTIVE ACTIVATION | G-cluartet oligodeoxynucleotide | GENE-REGULATION | MYELOID DIFFERENTIATION | G-QUARTET OLIGONUCLEOTIDES | CELL-GROWTH | DNA-BINDING ACTIVITY | SIGNALING INDUCES APOPTOSIS | cancer therapy | ONCOLOGY | EPIDERMAL-GROWTH-FACTOR | PHARMACOLOGY & PHARMACY | PHASE RESPONSE FACTOR | Neoplasms - metabolism | Cell Cycle Proteins - pharmacology | Transcriptional Activation - genetics | Cell Proliferation | Triterpenes - pharmacology | Apoptosis - drug effects | Humans | Cell Movement - physiology | Plasmids - pharmacology | Oligonucleotides - pharmacology | Angiogenesis Inducing Agents - pharmacology | Anticarcinogenic Agents - pharmacology | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Oligonucleotides, Antisense - pharmacology | Signal Transduction - genetics | Tyrphostins - pharmacology | src Homology Domains - physiology | Neoplasms - drug therapy | Animals | Ligands | Protein Conformation | Inhibitor of Apoptosis Proteins - pharmacology | Protein Kinase Inhibitors - pharmacology | Apoptosis - physiology | Protein-Tyrosine Kinases | Phosphopeptides - pharmacology
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6. Full Text Modulation of mast cell proteinase-activated receptor expression and IL-4 release by IL-12
by Zhang, Huiyun and Yang, Xiaoyu and Yang, Haiwei and Zhang, Zhongfang and Lin, Qing and Zheng, Yanshan and Chen, Shaoying and Yang, Pingchang and He, Shaoheng
Immunology and Cell Biology, ISSN 0818-9641, 10/2007, Volume 85, Issue 7, pp. 558 - 566
It has been recognized that protease‐activated receptors (PARs), interleukin (IL)‐4 and IL‐6 are involved in the pathogenesis of allergic diseases, and that... 
mast cell | IL‐4 | IL‐12 | trypsin | protease‐activated receptor | tryptase | IL-4 | Trypsin | Mast cell | Protease-activated receptor | IL-12 | Tryptase | SERINE PROTEINASES | THROMBIN RECEPTORS | HISTAMINE-RELEASE | INDUCTION | IMMUNOLOGY | HUMAN AIRWAYS | CELL BIOLOGY | SMOOTH-MUSCLE | INTERFERON-GAMMA | IN-VIVO | protease-activated receptor | VASCULAR ENDOTHELIAL-CELLS | INFLAMMATORY MEDIATORS | Receptors, Proteinase-Activated - metabolism | Nitriles - pharmacology | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - metabolism | RNA, Messenger - metabolism | Receptors, Proteinase-Activated - genetics | Trypsin - pharmacology | Mast Cells - metabolism | Flavonoids - pharmacology | Chromones - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Interleukin-12 - pharmacology | Butadienes - pharmacology | Cells, Cultured | Enzyme Inhibitors - pharmacology | Morpholines - pharmacology | Imidazoles - pharmacology | Tyrphostins - pharmacology | Mast Cells - drug effects | Gene Expression Regulation - drug effects | Interleukin-4 - secretion | Animals | Tryptases - pharmacology | Mice | Pyridines - pharmacology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Tyrphostins, pharmacology | Up-Regulation | Chromones, pharmacology | Trypsin, pharmacology | Humans | Imidazoles, pharmacology | Tryptases, pharmacology | Oligopeptides, pharmacology | Interleukin-12, pharmacology | Flow Cytometry | Pyridines, pharmacology | Polymerase Chain Reaction | Receptor, PAR-1, drug effects | Morpholines, pharmacology | RNA, Messenger, metabolism | Flavonoids, pharmacology | Receptor, PAR-2, drug effects | Receptors, Thrombin, drug effects | Enzyme-Linked Immunosorbent Assay | Signal Transduction | Butadienes, pharmacology | Down-Regulation | Mast Cells, drug effects | Interleukin-6, secretion | Nitriles, pharmacology | Reverse Transcriptase Polymerase Chain Reaction | Interleukin-4, secretion | Fluorescent Antibody Technique
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7. Full Text Sorafenib Sensitizes Glioma Cells to the BH3 Mimetic ABT-737 by Targeting MCL1 in a STAT3-Dependent Manner
by Kiprianova, Irina and Remy, Janina and Milosch, Nelli and Mohrenz, Isabelle V and Seifert, Volker and Aigner, Achim and Kögel, Donat
Neoplasia, ISSN 1476-5586, 2015, Volume 17, Issue 7, pp. 564 - 573
Abstract The oncogenic transcription factor signal transducer and activator of transcription 3 (STAT3) is overactivated in malignant glioma and plays a key... 
Oncology | MALIGNANT GLIOMA | CANCER-CELLS | IN-VITRO | GLIOBLASTOMA | ONCOLOGY | INDUCED APOPTOSIS | MOUSE MODEL | GROWTH | INHIBITOR | BCL-2 FAMILY | ADJUVANT TEMOZOLOMIDE | Niacinamide - analogs & derivatives | Humans | Myeloid Cell Leukemia Sequence 1 Protein - metabolism | Cell Survival - genetics | Apoptosis - genetics | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Gene Knockdown Techniques | Activating Transcription Factors - genetics | Biphenyl Compounds - pharmacology | Nitrophenols - pharmacology | Glioma - pathology | Antineoplastic Agents - pharmacology | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Peptide Hydrolases - metabolism | Cytochromes c - secretion | Tyrphostins - pharmacology | Sulfonamides - pharmacology | Piperazines - pharmacology | Myeloid Cell Leukemia Sequence 1 Protein - genetics | Cell Line, Tumor | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | Phenylurea Compounds - pharmacology | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Niacinamide - pharmacology | STAT3 Transcription Factor - antagonists & inhibitors
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8. Full Text β-amyloid monomers are neuroprotective
by Giuffrida, Maria Laura and Caraci, Filippo and Pignataro, Bruno and Cataldo, Sebastiano and De Bona, Paolo and Bruno, Valeria and Molinaro, Gemma and Pappalardo, Giuseppe and Messina, Angela and Palmigiano, Angelo and Garozzo, Domenico and Nicoletti, Ferdinando and Rizzarelli, Enrico and Copani, Agata
Journal of Neuroscience, ISSN 0270-6474, 08/2009, Volume 29, Issue 34, pp. 10582 - 10587
The 42-aa-long beta-amyloid protein-A beta(1-42)-is thought to play a central role in the pathogenesis of Alzheimer's disease (AD) (Walsh and Selkoe, 2007).... 
SIGNAL-TRANSDUCTION | INSULIN-RECEPTOR | HUMAN BRAIN | PHOSPHORYLATION | ALZHEIMERS-DISEASE | CASCADES | INHIBITOR | SYNAPTIC PLASTICITY | NEUROSCIENCES | PEPTIDE | OLIGOMERS | Butadienes - pharmacology | Podophyllotoxin - pharmacology | Nitriles - pharmacology | Embryo, Mammalian | Amyloid beta-Peptides - pharmacology | Cells, Cultured | Enzyme Inhibitors - pharmacology | Rats | Peptide Fragments - pharmacology | Tyrphostins - pharmacology | Cerebral Cortex - cytology | Dose-Response Relationship, Drug | Peptide Fragments - chemistry | Animals | Excitatory Amino Acid Agonists - toxicity | Neuroprotective Agents - pharmacology | Analysis of Variance | Amyloid beta-Peptides - chemistry | Cell Death - drug effects | Neurons - drug effects | N-Methylaspartate - toxicity | Podophyllotoxin - analogs & derivatives | Index Medicus | Brief Communications
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9. Full Text Mechanisms of caspase-1 activation by P2X7 receptor-mediated K+ release
by J. Michelle Kahlenberg and George R. Dubyak
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 05/2004, Volume 286, Issue 5, pp. 1100 - 1108
The mechanisms underlying caspase-1 activation and IL-1β processing during inflammatory activation of monocytes and macrophages are not well defined. Here, we... 
ASC | IL-1β | Infammation | AG-126 | Bromoenol lactone | Potassium - metabolism | Cercopithecus aethiops | Caspase 1 - metabolism | Pyrones - pharmacology | Adenosine Triphosphate - pharmacology | Cytoskeletal Proteins - pharmacology | Ionophores - pharmacology | Cell Line | Interleukin-1 - metabolism | Enzyme Inhibitors - pharmacology | Phosphodiesterase Inhibitors - pharmacology | Receptors, Purinergic P2 - physiology | Tyrphostins - pharmacology | Recombinant Proteins - pharmacology | Macrophages - enzymology | Naphthalenes - pharmacology | Receptors, Purinergic P2X7 | Macrophages - metabolism | Animals | Apoptosis Regulatory Proteins | Cell-Free System | CARD Signaling Adaptor Proteins | Mice | Nigericin - pharmacology | Enzyme Activation | COS Cells
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10. Full Text The bile acid receptor TGR5 does not interact with β-arrestins or traffic to endosomes but transmits sustained signals from plasma membrane rafts
by Jensen, Dane D and Godfrey, Cody B and Niklas, Christian and Canals, Meritxell and Kocan, Martina and Poole, Daniel P and Murphy, Jane E and Alemi, Farzad and Cottrell, Graeme S and Korbmacher, Christoph and Lambert, Nevin A and Bunnett, Nigel W and Corvera, Carlos U
Journal of Biological Chemistry, ISSN 0021-9258, 08/2013, Volume 288, Issue 32, pp. 22942 - 22960
TGR5 is a G protein-coupled receptor that mediates bile acid (BA) effects on energy balance, inflammation, digestion, and sensation. The mechanisms and... 
GROWTH-FACTOR RECEPTOR | BIOCHEMISTRY & MOLECULAR BIOLOGY | GPBAR1 TGR5 | DEPENDENT ENDOCYTOSIS | PROTEIN-COUPLED RECEPTORS | RESONANCE ENERGY-TRANSFER | KINASE ACTIVATION | MU-OPIOID RECEPTOR | BETA-ADRENERGIC RECEPTOR | ACTIVATED RECEPTOR-2 | EGF RECEPTOR | Cholagogues and Choleretics - pharmacology | Phenylalanine - analogs & derivatives | Receptors, G-Protein-Coupled - metabolism | Membrane Microdomains - metabolism | Phenylalanine - pharmacology | Humans | ErbB Receptors - genetics | Oleanolic Acid - pharmacology | Arrestins - genetics | Protein Transport - physiology | Protein Transport - drug effects | G-Protein-Coupled Receptor Kinase 2 - genetics | G-Protein-Coupled Receptor Kinase 2 - metabolism | Arrestins - metabolism | beta-Cyclodextrins - pharmacology | Endosomes - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | HEK293 Cells | Antineoplastic Agents - pharmacology | Cyclic AMP - genetics | Cyclic AMP - metabolism | ErbB Receptors - antagonists & inhibitors | ErbB Receptors - metabolism | Endosomes - genetics | Mitogen-Activated Protein Kinase 3 - genetics | Endocytosis - drug effects | Enzyme Inhibitors - pharmacology | Thiophenes - pharmacology | Tyrphostins - pharmacology | Endocytosis - physiology | Arrestins - antagonists & inhibitors | G-Protein-Coupled Receptor Kinase 5 - metabolism | Deoxycholic Acid - pharmacology | Mitogen-Activated Protein Kinase 3 - metabolism | beta-Arrestin 2 | beta-Arrestin 1 | beta-Arrestins | Receptors, G-Protein-Coupled - genetics | Quinazolines - pharmacology | G-Protein-Coupled Receptor Kinase 5 - genetics | Membrane Microdomains - genetics | Mitogen-Activated Protein Kinase 1 - metabolism | Lipid Raft | Bile Acid | Endocytosis | G Protein-coupled Receptors (GPCR) | Arrestin | Signal Transduction
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11. Full Text The immune modulator FTY720 targets sphingosine-kinase-dependent migration of human monocytes in response to amyloid beta-protein and its precursor
by Kaneider, NC and Lindner, J and Feistritzer, C and Sturn, DH and Mosheimer, BA and Djanani, AM and Wiedermann, CJ
FASEB JOURNAL, ISSN 0892-6638, 06/2004, Volume 18, Issue 9, pp. 1309 - 1309
Accumulation of inflammatory mononuclear phagocytes in Alzheimer's senile plaques, a hallmark of the innate immune response to beta-amyloid fibrils, can... 
ACTIVATION | G-protein coupled receptors | Alzheimer disease | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | immunosuppression | NEUTROPHILS | sphingosine-1-phosphate receptors | MESSENGER | PEPTIDE | CELL BIOLOGY | FIBRILS | MICROGLIA | SPHINGOSINE-1-PHOSPHATE | BIOLOGY | leukocytes | T-CELL CHEMOTAXIS | 1-PHOSPHATE | Phosphotransferases (Alcohol Group Acceptor) - physiology | Amyloid beta-Peptides - pharmacology | Humans | Maleimides - pharmacology | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | RNA, Messenger - biosynthesis | Bombesin - pharmacology | Chemotaxis, Leukocyte - drug effects | Protein Processing, Post-Translational - drug effects | Vasoactive Intestinal Peptide - pharmacology | Neuropeptides - pharmacology | N-Formylmethionine Leucyl-Phenylalanine - pharmacology | Receptors, Lysosphingolipid - genetics | Indoles - pharmacology | Cholera Toxin - pharmacology | Heterotrimeric GTP-Binding Proteins - physiology | Phosphorylation - drug effects | Drug Evaluation, Preclinical | Pertussis Toxin - pharmacology | Propylene Glycols - pharmacology | Leukocytes, Mononuclear - drug effects | Calcitonin Gene-Related Peptide - pharmacology | Enzyme Inhibitors - pharmacology | Secretogranin II | Fingolimod Hydrochloride | Receptors, Lysosphingolipid - physiology | Tyrphostins - pharmacology | 1-Methyl-3-isobutylxanthine - pharmacology | Gene Expression Regulation - drug effects | Sphingosine - pharmacology | Cell Movement - drug effects | Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors | Sphingosine - analogs & derivatives | Androstadienes - pharmacology | Receptors, Lysosphingolipid - agonists | Leukocytes, Mononuclear - cytology | Protein Kinase Inhibitors - pharmacology | Immunologic Factors - pharmacology | Receptors, Lysosphingolipid - biosynthesis | Staurosporine - pharmacology | Amyloid beta-Protein Precursor - pharmacology
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12. Full Text gp91phox-Containing NADPH Oxidase Mediates Endothelial Dysfunction in Renovascular Hypertension
by Jung, O and Schreiber, J.G and Geiger, H and Pedrazzini, T and Busse, R and Brandes, Ralf P
Circulation, ISSN 0009-7322, 04/2004, Volume 109, Issue 14, pp. 1795 - 1801
Background - Isoforms of the NADPH oxidase contribute to vascular superoxide anion (.O-2(-)) formation and limit NO bioavailability. We hypothesized that the... 
Hypertension | Stress, oxidative | Angiotensin | Endothelium | endothelium | PROTEIN-KINASE-C | CARDIAC & CARDIOVASCULAR SYSTEMS | stress, oxidative | SUPEROXIDE-PRODUCTION | INVOLVEMENT | ANGIOTENSIN-II | DEFICIENT MICE | NAD(P)H OXIDASE | DISEASE | angiotensin | TETRAHYDROBIOPTERIN | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | hypertension | EXPRESSION | SMOOTH-MUSCLE CELLS | Angiotensin II - blood | Male | 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt - pharmacology | Hypertension, Renovascular - physiopathology | Quinazolines | Endothelium, Vascular - enzymology | Glycoproteins - pharmacology | Cytochromes b - deficiency | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Superoxides - metabolism | Aorta | Indoles - pharmacology | Membrane Glycoproteins | Cardiomyopathy, Hypertrophic - etiology | Organ Culture Techniques | Disease Models, Animal | Polyethylene Glycols - pharmacology | NADPH Oxidases | Superoxide Dismutase - pharmacology | Vasodilator Agents - pharmacology | Acetylcholine - pharmacology | Hypertension, Renovascular - enzymology | Mice, Inbred C57BL | Endothelium, Vascular - physiopathology | Enzyme Inhibitors - pharmacology | Protein Kinase C - antagonists & inhibitors | Tyrphostins - pharmacology | Antioxidants - pharmacology | NADPH Oxidase 2 | Mice, Knockout | Proto-Oncogene Proteins c-akt | Animals | Hypertension, Renovascular - complications | Bacterial Toxins - pharmacology | Cytochromes b - genetics | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Mice | Vasodilation - drug effects | Nitric Oxide - metabolism | Cytochromes b - physiology
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13. Full Text Diverse intracellular pathogens activate type III interferon expression from peroxisomes
by Odendall, Charlotte and Dixit, Evelyn and Stavru, Fabrizia and Bierne, Helene and Franz, Kate M and Durbin, Ann Fiegen and Boulant, Steeve and Gehrke, Lee and Cossart, Pascale and Kagan, Jonathan C
Nature Immunology, ISSN 1529-2908, 2014, Volume 15, Issue 8, pp. 717 - 726
Type I interferon responses are considered the primary means by which viral infections are controlled in mammals. Despite this view, several pathogens activate... 
INDEPENDENT ANTIVIRAL RESPONSE | HEPATITIS-C VIRUS | PATHWAY | IFN-LAMBDA-S | GENES | CELL LINE | INFECTION | IMMUNOLOGY | MEMBRANE-PROTEINS | DENGUE VIRUS | INNATE IMMUNITY | Interferons - biosynthesis | Cyclohexanes - pharmacology | Humans | Interferons - immunology | Intestinal Mucosa - cytology | Signal Transduction - immunology | RNA Interference | Intestinal Mucosa - immunology | Reoviridae - immunology | Antineoplastic Agents - pharmacology | Cell Differentiation | Janus Kinase 2 - antagonists & inhibitors | Cell Line | DEAD Box Protein 58 | Peroxisomes - immunology | Reoviridae Infections - immunology | Enzyme Inhibitors - pharmacology | Janus Kinase 2 - genetics | p38 Mitogen-Activated Protein Kinases - genetics | Tyrphostins - pharmacology | Vidarabine - analogs & derivatives | Immunity, Innate | STAT1 Transcription Factor - antagonists & inhibitors | STAT1 Transcription Factor - immunology | Vidarabine - pharmacology | Animals | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | DEAD-box RNA Helicases - immunology | Benzimidazoles - pharmacology | Mice | RNA, Small Interfering | Pyridones - pharmacology | Physiological research | Interferon | Immune response | Research | Properties | Life Sciences
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14. Full Text Transactivation of Epidermal Growth Factor Receptor Mediates Catecholamine-Induced Growth of Vascular Smooth Muscle
by Zhang, Hua and Chalothorn, Dan and Jackson, Leslie F and Lee, David C and Faber, James E
Circulation Research, ISSN 0009-7330, 11/2004, Volume 95, Issue 10, pp. 989 - 997
Stimulation of α1-adrenoceptors induces proliferation of vascular smooth muscle cells (SMCs) and contributes to arterial remodeling. Although activation of... 
Vascular smooth muscle cell proliferation | Signal transduction | α-adrenergic receptor | Reactive oxygen species | Metalloproteinase | ADVENTITIAL FIBROBLASTS | CARDIAC & CARDIOVASCULAR SYSTEMS | signal transduction | HB-EGF | metalloproteinase | PROTEIN-COUPLED RECEPTORS | ANGIOTENSIN-II | CELL REPLICATION | vascular smooth muscle cell proliferation | MATRIX METALLOPROTEINASES |