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Plant Physiology, ISSN 0032-0889, 3/2012, Volume 158, Issue 3, pp. 1451 - 1462
To analyze the copper-induced cross talk among calcium, nitric oxide (NO), and hydrogen peroxide (H₂O₂) and the calciumdependent activation of gene expression,... 
Tricarboxylic acid cycle | Antioxidants | Enzymes | Calcium channels | Dehydrogenases | Calcium | Oxides | Plants | Copper | ENVIRONMENTAL STRESS AND ADAPTATION TO STRESS | Plant cells | RELEASE CHANNELS | S-NITROSYLATION | NICOTIANA-PLUMBAGINIFOLIA CELLS | ANTAGONISTS INHIBIT | SYNTHASE ACTIVITY | ISOCITRATE DEHYDROGENASE | ELICITOR CRYPTOGEIN | ENDOPLASMIC-RETICULUM | ABSCISIC-ACID | PYRUVATE-DEHYDROGENASE COMPLEX | PLANT SCIENCES | Protein Kinases - metabolism | Antimycin A - metabolism | Calmodulin - genetics | Electron Transport | Protein Kinases - genetics | Ryanodine - metabolism | Calcium Channels - metabolism | Calcium - metabolism | Transcriptional Activation | Nitric Oxide Synthase - antagonists & inhibitors | Piperazines - metabolism | Carbolines - metabolism | Antimycin A - pharmacology | Mitochondria - genetics | Time Factors | Gene Expression Regulation, Plant | Plant Proteins - metabolism | Ulva - metabolism | Calcium Channel Blockers - metabolism | Calcium Channels - genetics | Ulva - genetics | Chloroplasts - genetics | Ryanodine - pharmacology | Calmodulin - metabolism | Cell Survival | Copper - pharmacology | Mitochondria - metabolism | Calcium Channel Blockers - pharmacology | Piperazines - pharmacology | Chloroplasts - metabolism | Citric Acid Cycle | Hydrogen Peroxide - metabolism | Plant Proteins - genetics | Ulva - drug effects | Nitric Oxide Synthase - metabolism | Enzyme Activation | Nitric Oxide - metabolism | Carbolines - pharmacology | Hydrogen peroxide | Calcium, Dietary | Marine algae | Physiological aspects | Genetic aspects | Research | Gene expression | Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 04/2013, Volume 288, Issue 17, pp. 11920 - 11929
Journal Article
Cancer Cell, ISSN 1535-6108, 2006, Volume 10, Issue 5, pp. 389 - 399
Since apoptosis is impaired in malignant cells overexpressing prosurvival Bcl-2 proteins, drugs mimicking their natural antagonists, BH3-only proteins, might... 
CELLCYCLE | SURVIVAL | SELICICLIB CYC202 | R-ROSCOVITINE | ONCOLOGY | SMALL-MOLECULE INHIBITORS | DOWN-REGULATION | DEATH | KINASE INHIBITOR | FAMILY PROTEINS | MULTIPLE-MYELOMA CELLS | BH3-ONLY PROTEINS | bcl-2-Associated X Protein - chemistry | Humans | Leukemia, Myeloid, Acute - metabolism | Nitrophenols - metabolism | bcl-2 Homologous Antagonist-Killer Protein - genetics | Male | Piperazines - metabolism | Neoplasm Proteins - metabolism | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Biphenyl Compounds - metabolism | Biphenyl Compounds - therapeutic use | Recombinant Fusion Proteins - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Biphenyl Compounds - pharmacology | Nitrophenols - pharmacology | RNA Interference | Nitrophenols - therapeutic use | Leukemia, Myeloid, Acute - drug therapy | Proto-Oncogene Proteins c-bcl-2 - chemistry | bcl-2-Associated X Protein - genetics | Disease Models, Animal | Fibroblasts - metabolism | Protein Structure, Tertiary | Cytokines - metabolism | Leukemia, Myeloid, Acute - pathology | Mice, Inbred C57BL | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Mice, Transgenic | Piperazines - therapeutic use | Sulfonamides - pharmacology | Piperazines - pharmacology | Animals | Sulfonamides - therapeutic use | Myeloid Cell Leukemia Sequence 1 Protein | Sulfonamides - metabolism | Recombinant Fusion Proteins - genetics | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | Fibroblasts - cytology | Mice | Proto-Oncogene Proteins c-bcl-2 - genetics | Apoptosis | Proteins | Lymphomas | Analysis | Index Medicus
Journal Article
Cell Death and Disease, ISSN 2041-4889, 2014, Volume 5, Issue 5, pp. e1212 - e1212
Oxidative stress serves as an important regulator of both apoptosis and metabolic reprogramming in tumor cells. Chaetocin, a histone methyltransferase... 
YAP | ATM | Metabolism | JNK | Glioblastoma | ROS | YES-ASSOCIATED PROTEIN | GLIOMA-CELLS | ACTIVATION | DNA-DAMAGE | CANCER | CELL BIOLOGY | GROWTH | KAPPA-B AXIS | metabolism | UP-REGULATION | GLIOBLASTOMA CELLS | Reactive Oxygen Species - metabolism | Ataxia Telangiectasia Mutated Proteins - metabolism | Apoptosis - drug effects | Humans | Brain Neoplasms - pathology | JNK Mitogen-Activated Protein Kinases - metabolism | Phosphoproteins - metabolism | DNA-Binding Proteins - metabolism | Dose-Response Relationship, Drug | Glioma - genetics | Transfection | RNA Interference | Time Factors | Adenosine Triphosphate - metabolism | Glioma - pathology | Antineoplastic Agents - pharmacology | Brain Neoplasms - enzymology | Tumor Suppressor Proteins - metabolism | Glioma - enzymology | Pyruvate Kinase - metabolism | Lactic Acid - metabolism | Brain Neoplasms - genetics | Nuclear Proteins - metabolism | Phosphoproteins - genetics | Brain Neoplasms - drug therapy | Piperazines - pharmacology | Xenograft Model Antitumor Assays | p300-CBP Transcription Factors - metabolism | Tumor Protein p73 | Animals | Signal Transduction - drug effects | Tumor Burden - drug effects | Mice, Nude | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Glucose - metabolism | Cell Proliferation - drug effects | Mice | Enzyme Activation | Oxidative Stress - drug effects | Adaptor Proteins, Signal Transducing - metabolism | Hexokinase - metabolism | Glioma - drug therapy | Index Medicus | Original
Journal Article
Toxicology, ISSN 0300-483X, 2005, Volume 216, Issue 2, pp. 154 - 167
Many adverse drug reactions are caused by the cytochrome P450 (CYP) dependent activation of drugs into reactive metabolites. In order to reduce attrition due... 
Reactive metabolites | Cytotoxicity | Metabolism-mediated toxicity | CYP3A4 | In vitro screening | Adverse drug reactions (ADRs) | CYTOCHROME-P450 | MEDIATED CYTOTOXICITY | HUMAN HEPATOCYTE CULTURES | in vitro screening | CARBAMAZEPINE | adverse drug reactions (ADRs) | STABLE EXPRESSION | INDUCTION | metabolism-mediated toxicity | IDIOSYNCRATIC DRUG-REACTIONS | CHINESE-HAMSTER CELLS | HEPG2 CELLS | PHARMACOLOGY & PHARMACY | TOXICOLOGY | reactive metabolites | HUMAN-LIVER-MICROSOMES | cytotoxicity | Microsomes - metabolism | Thiazoles - metabolism | Cytochrome P-450 Enzyme Inhibitors | Cytochrome P-450 CYP3A | Coculture Techniques | Humans | Thiazolidinediones - toxicity | Cytochrome P-450 Enzyme System - metabolism | Isoniazid - toxicity | Xenobiotics - toxicity | Chromans - metabolism | Flutamide - metabolism | Triazolam - toxicity | Microsomes - drug effects | Triazolam - metabolism | Adenosine Triphosphate - metabolism | Carbamazepine - toxicity | Toxicity Tests - methods | Xenobiotics - metabolism | Cell Culture Techniques | Cell Survival - drug effects | Albendazole - toxicity | Tamoxifen - toxicity | Dapsone - metabolism | Dapsone - toxicity | Cell Line, Tumor | Glutathione - chemistry | Troglitazone | Buthionine Sulfoximine - pharmacology | Quinidine - toxicity | Amitriptyline - toxicity | Glutathione - metabolism | Flutamide - toxicity | Substrate Specificity | Piperazines - metabolism | Piperazines - toxicity | Ochratoxins - metabolism | Xenobiotics - chemistry | Tetrazolium Salts - metabolism | Carbamazepine - metabolism | Quinidine - metabolism | Tamoxifen - metabolism | Amitriptyline - metabolism | Glutathione - antagonists & inhibitors | Enzyme Activation - drug effects | Thiazolidinediones - metabolism | Ochratoxins - toxicity | Thiazoles - toxicity | Animals | Albendazole - metabolism | Chromans - toxicity | Isoniazid - metabolism | Phosphates | Metabolites | Ketoconazole | Cytochrome P-450 | Control systems | Xenobiotics | Glutathione | Index Medicus
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 04/2010, Volume 30, Issue 4, pp. 758 - 765
OBJECTIVE—Diet-induced obesity (DIO) in mice causes vascular inflammation and insulin resistance that are accompanied by decreased endothelial-derived NO... 
ENOS | Nitric oxide | Vascular inflammation | nitric oxide | eNOS | ACTIVATED PROTEIN-KINASE | SILDENAFIL | IKK-BETA | ALPHA | ADHESION MOLECULES | NITRIC-OXIDE PRODUCTION | INHIBITION | ENDOTHELIAL-CELLS | vascular inflammation | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | NF-KAPPA-B | EXPRESSION | Humans | Phosphodiesterase 5 Inhibitors | Male | NF-kappa B - metabolism | Insulin Receptor Substrate Proteins - metabolism | Aortic Diseases - metabolism | Sildenafil Citrate | Inflammation - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Disease Models, Animal | Endothelial Cells - metabolism | Down-Regulation | Enzyme Inhibitors - pharmacology | Aorta, Thoracic - metabolism | Cell Adhesion Molecules - metabolism | Inflammation - etiology | Nitric Oxide Synthase Type III - genetics | Piperazines - pharmacology | Mice, Knockout | Nitric Oxide Synthase Type III - antagonists & inhibitors | Insulin - metabolism | Cyclic GMP - metabolism | Signal Transduction - drug effects | Inflammation - prevention & control | Mice | Endothelial Cells - enzymology | Palmitic Acid - metabolism | Phosphorylation | Phosphatidylinositol 3-Kinases - metabolism | Sulfones - pharmacology | I-kappa B Kinase - metabolism | Dietary Fats | Inflammation Mediators - metabolism | Aorta, Thoracic - drug effects | Nitric Oxide Donors - pharmacology | Nitric Oxide Synthase Type III - metabolism | Cyclic Nucleotide Phosphodiesterases, Type 5 - metabolism | Purines - pharmacology | Mice, Inbred C57BL | Cells, Cultured | Insulin Resistance | Phosphodiesterase Inhibitors - pharmacology | Aorta, Thoracic - physiopathology | Aortic Diseases - physiopathology | Animals | Nitric Oxide - metabolism | Aortic Diseases - etiology | Endothelial Cells - drug effects | Inflammation - physiopathology | Index Medicus
Journal Article
ChemMedChem, ISSN 1860-7179, 04/2017, Volume 12, Issue 7, pp. 487 - 501
Sulfoximines have gained considerable recognition as an important structural motif in drug discovery of late. In particular, the clinical kinase inhibitors for... 
kinase inhibitors | pharmacophores | sulfoximines | drug design | medicinal chemistry | PHOSPHODIESTERASE-5 INHIBITORS | CHEMISTRY, MEDICINAL | ASYMMETRIC-SYNTHESIS | DIELS-ALDER REACTIONS | DEPENDENT KINASE INHIBITOR | BREAST-CANCER | POTENT INHIBITOR | STRUCTURAL BASIS | CDK4/6 INHIBITOR | PHARMACOLOGY & PHARMACY | ERECTILE DYSFUNCTION | Estradiol - analogs & derivatives | Sulfoxides - chemical synthesis | Cyclin-Dependent Kinases - metabolism | Ataxia Telangiectasia Mutated Proteins - metabolism | Imatinib Mesylate - chemical synthesis | Pyrazoles - chemical synthesis | Pyridines - chemistry | Imatinib Mesylate - metabolism | Piperazines - metabolism | Piperazines - chemistry | Aminopyridines - metabolism | Fulvestrant | Aminopyridines - chemistry | Protein Kinase Inhibitors - chemistry | Pyrazoles - chemistry | Vardenafil Dihydrochloride - chemistry | Drug Design | Ataxia Telangiectasia Mutated Proteins - antagonists & inhibitors | Cyclin-Dependent Kinases - antagonists & inhibitors | Purines - chemical synthesis | Estradiol - metabolism | Protein Kinase Inhibitors - chemical synthesis | Piperidines - chemistry | Piperidines - metabolism | Purines - metabolism | Pyridines - chemical synthesis | Pyrazoles - metabolism | Piperidines - chemical synthesis | Imatinib Mesylate - chemistry | Vardenafil Dihydrochloride - metabolism | Aminopyridines - chemical synthesis | Sulfoxides - chemistry | Estradiol - chemistry | Purines - chemistry | Pyridines - metabolism | Vardenafil Dihydrochloride - chemical synthesis | Sulfoxides - metabolism | Piperazines - chemical synthesis | Estradiol - chemical synthesis | Protein Kinase Inhibitors - metabolism | Drug discovery | Chemical properties | Pharmaceutical industry | Index Medicus | Full Paper | Full Papers
Journal Article
Neurotoxicology, ISSN 0161-813X, 03/2013, Volume 35, Issue 1, pp. 30 - 40
► Neoechinulin A, an alkaloid was isolated form marine fungal strain sp. ► Neoechinulin A, suppressed the production of pro-inflammatory mediators in microglia... 
Neoechinulin A | Neuroinflammation | Reactive oxygen species | Pro-inflammatory mediators | Amyloid-β | Alzheimer's disease | OXIDATIVE STRESS | ALZHEIMERS-DISEASE | MODEL | NEUROSCIENCES | MAPK SIGNALING PATHWAYS | A-BETA | PC12 CELL | THERAPEUTIC TARGETS | PHARMACOLOGY & PHARMACY | TOXICOLOGY | INDUCED CYTOTOXICITY | NF-KAPPA-B | Amyloid-beta | Tumor Necrosis Factor-alpha - metabolism | Inflammation - pathology | Microglia - metabolism | Neurons - pathology | Phosphorylation | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Tumor Necrosis Factor-alpha - genetics | NF-kappa B - metabolism | Interleukin-1beta - genetics | PC12 Cells | Dose-Response Relationship, Drug | Inflammation - metabolism | Neuroprotective Agents - pharmacology | Cyclooxygenase 2 - genetics | Interleukin-1beta - metabolism | Amyloid beta-Peptides - metabolism | Inflammation Mediators - metabolism | Microglia - pathology | Neurons - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | MAP Kinase Kinase Kinase 5 - metabolism | Neurons - drug effects | Interleukin-6 - metabolism | Cytoprotection | Peptide Fragments - metabolism | Interleukin-6 - genetics | Microglia - drug effects | Anti-Inflammatory Agents - pharmacology | Reactive Nitrogen Species - metabolism | Gene Expression Regulation | Rats | Piperazines - pharmacology | Dinoprostone - metabolism | Animals | Nitric Oxide Synthase Type II - genetics | Signal Transduction - drug effects | Indole Alkaloids - pharmacology | Cell Communication - drug effects | Cyclooxygenase 2 - metabolism | Inflammation - genetics | Inflammation - prevention & control | Mice | Oxidative Stress - drug effects | Nitric Oxide Synthase Type II - metabolism | Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 06/2006, Volume 116, Issue 6, pp. 1561 - 1570
Metastasis is the major cause of cancer morbidity, but strategies for direct interference with invasion processes are lacking. Dedifferentiated, late-stage... 
BREAST-CANCER | MEDICINE, RESEARCH & EXPERIMENTAL | FACTOR-BETA | 3D CULTURES | GROWTH-FACTOR-RECEPTOR | TRANSFORMED PHENOTYPE | EPITHELIAL-MESENCHYMAL TRANSITIONS | CELL-LINES | NF-KAPPA-B | MOLECULAR-MECHANISMS | INCREASED MALIGNANCY | Humans | ras Proteins - metabolism | Mammary Tumor Virus, Mouse - metabolism | Piperazines - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Mammary Neoplasms, Experimental - metabolism | Recombinant Fusion Proteins - metabolism | Pyrimidines - metabolism | Breast Neoplasms - metabolism | Antineoplastic Agents - metabolism | Epithelial Cells - physiology | Neoplasm Metastasis | Mammary Neoplasms, Experimental - pathology | Female | Epithelial Cells - cytology | Cell Differentiation - physiology | Receptor, Platelet-Derived Growth Factor beta - metabolism | Autocrine Communication | Receptor, Platelet-Derived Growth Factor alpha - metabolism | Mice, Transgenic | Imatinib Mesylate | Animals | Transforming Growth Factor beta - genetics | Breast Neoplasms - pathology | Mice, Nude | Cell Line, Tumor | Mesoderm - physiology | Recombinant Fusion Proteins - genetics | Signal Transduction - physiology | Mice | Benzamides | Enzyme Activation | Mammary Tumor Virus, Mouse - genetics | Transforming Growth Factor beta - metabolism | Apoptosis | Protein Kinase Inhibitors - metabolism | Medicine, Experimental | Medical research | Breast cancer | Research | Metastasis | Drug therapy | Index Medicus | Abridged Index Medicus
Journal Article
Cancer Cell, ISSN 1535-6108, 2006, Volume 10, Issue 5, pp. 375 - 388
BCL-2 proteins are critical for cell survival and are overexpressed in many tumors. ABT-737 is a small-molecule BH3 mimetic that exhibits single-agent activity... 
CELLCYCLE | PROGRAMMED CELL-DEATH | CANCER-CELLS | STEM-CELLS | PROAPOPTOTIC ACTIVITY | ONCOLOGY | X-L | ACUTE MYELOGENOUS LEUKEMIA | IN-VIVO | MITOCHONDRIAL-MEMBRANE | BCL-2 FAMILY-MEMBERS | BH3-ONLY PROTEINS | RNA, Small Interfering - genetics | bcl-2-Associated X Protein - chemistry | Humans | Leukemia, Myeloid, Acute - metabolism | Nitrophenols - metabolism | bcl-2 Homologous Antagonist-Killer Protein - genetics | Piperazines - metabolism | Neoplasm Proteins - metabolism | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Biphenyl Compounds - metabolism | Biphenyl Compounds - therapeutic use | Recombinant Fusion Proteins - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Nitrophenols - therapeutic use | Hematopoietic Stem Cells - physiology | Leukemia, Myeloid, Acute - drug therapy | Proto-Oncogene Proteins c-bcl-2 - chemistry | Dimerization | bcl-2-Associated X Protein - genetics | Protein Structure, Tertiary | Cell Line | bcl-2-Associated X Protein - metabolism | Piperazines - therapeutic use | Animals | Sulfonamides - therapeutic use | Myeloid Cell Leukemia Sequence 1 Protein | Sulfonamides - metabolism | Recombinant Fusion Proteins - genetics | Protein Conformation | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | Mice | Apoptosis - physiology | Drug Resistance, Neoplasm - physiology | Proto-Oncogene Proteins c-bcl-2 - genetics | RNA, Small Interfering - metabolism | Proteins | Oncology, Experimental | Lung cancer | Bone marrow | Transplantation | Lymphomas | Research | Hematopoietic stem cells | Cancer | Apoptosis | Index Medicus
Journal Article
Nature Structural and Molecular Biology, ISSN 1545-9993, 07/2016, Volume 23, Issue 7, pp. 647 - 655
The opposing activities of 53BP1 and BRCA1 influence pathway choice in DNA double-strand-break repair. How BRCA1 counteracts the inhibitory effect of 53BP1 on... 
STRAND BREAK REPAIR | RING-RING COMPLEX | TUMOR SUPPRESSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | REPAIR PATHWAY CHOICE | BRCA1 | REMODELING ENZYME | CELL BIOLOGY | E3 LIGASE | BIOPHYSICS | END RESECTION | HOMOLOGOUS RECOMBINATION | FUN30 | Chromatin - metabolism | DNA, Neoplasm - metabolism | Humans | Gene Expression Regulation, Neoplastic | Ubiquitin - metabolism | DNA Breaks, Double-Stranded | Ubiquitination - drug effects | BRCA1 Protein - metabolism | Tumor Suppressor Proteins - genetics | Cloning, Molecular | Escherichia coli - metabolism | Binding Sites | Chromatin - drug effects | DNA Helicases - genetics | Chromatin - chemistry | Tumor Suppressor p53-Binding Protein 1 - metabolism | Recombinant Proteins - metabolism | Gene Expression | Recombinational DNA Repair | Tumor Suppressor Proteins - metabolism | Tumor Suppressor p53-Binding Protein 1 - genetics | Signal Transduction | Ubiquitin-Protein Ligases - metabolism | Models, Molecular | Recombinant Proteins - genetics | Ubiquitin - genetics | Piperazines - pharmacology | DNA Cleavage - drug effects | BRCA1 Protein - genetics | DNA Helicases - metabolism | Phthalazines - pharmacology | Histones - genetics | Escherichia coli - genetics | Protein Binding | DNA, Neoplasm - genetics | HeLa Cells | Histones - metabolism | Ubiquitin-Protein Ligases - genetics | Camptothecin - pharmacology | Breast cancer | BRCA mutations | DNA repair | Analysis | Risk factors | Enzymes | Protein expression | Chromatin | DNA damage | Index Medicus
Journal Article