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1. Full Text Defective Mitophagy in XPA via PARP-1 Hyperactivation and NAD+/SIRT1 Reduction
by Fang, Evandro Fei and Scheibye-Knudsen, Morten and Brace, Lear E and Kassahun, Henok and SenGupta, Tanima and Nilsen, Hilde and Mitchell, James R and Croteau, Deborah L and Bohr, Vilhelm A
Cell, ISSN 0092-8674, 05/2014, Volume 157, Issue 4, pp. 882 - 896
Mitochondrial dysfunction is a common feature in neurodegeneration and aging. We identify mitochondrial dysfunction in xeroderma pigmentosum group A (XPA), a... 
XERODERMA-PIGMENTOSUM | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE MODEL | MITOCHONDRIA | COCKAYNE-SYNDROME | UNCOUPLING PROTEIN-2 | AUTOPHAGY | PIGMENTOSUM GROUP-A | DNA-REPAIR | DAMAGE | PARKINSONS-DISEASE | CELL BIOLOGY | Protein Kinases - metabolism | Sirtuin 1 - metabolism | Xeroderma Pigmentosum - physiopathology | Cell Line | Xeroderma Pigmentosum Group A Protein - metabolism | Xeroderma Pigmentosum - metabolism | Humans | Rats | Autophagy | Mitochondrial Degradation | Caenorhabditis elegans | Poly(ADP-ribose) Polymerases - metabolism | Animals | Ion Channels - metabolism | Mitochondrial Proteins - metabolism | Aging | Mice | Uncoupling Protein 2 | Apoptosis | Index Medicus
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2. Full Text The NAD+/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling
by Mouchiroud, Laurent and Houtkooper, Riekelt H and Moullan, Norman and Katsyuba, Elena and Ryu, Dongryeol and Cantó, Carles and Mottis, Adrienne and Jo, Young-Suk and Viswanathan, Mohan and Schoonjans, Kristina and Guarente, Leonard and Auwerx, Johan
Cell, ISSN 0092-8674, 07/2013, Volume 154, Issue 2, pp. 430 - 441
NAD is an important cofactor regulating metabolic homeostasis and a rate-limiting substrate for sirtuin deacylases. We show that NAD levels are reduced in aged... 
TRANSCRIPTION FACTORS | OXIDATIVE STRESS | CAENORHABDITIS-ELEGANS | ENERGY-EXPENDITURE | HIGH-FAT DIET | BIOCHEMISTRY & MOLECULAR BIOLOGY | EXTENDS LIFE-SPAN | POLY(ADP-RIBOSE) POLYMERASE-1 | DIET-INDUCED OBESITY | C. ELEGANS | CALORIE RESTRICTION | CELL BIOLOGY | Sirtuin 1 - metabolism | Reactive Oxygen Species - metabolism | Signal Transduction | Caenorhabditis elegans Proteins - metabolism | Mitochondria - metabolism | Hepatocytes - metabolism | Longevity | Unfolded Protein Response | Poly(ADP-ribose) Polymerase Inhibitors | Sirtuin 1 - genetics | Transcription Factors - metabolism | Caenorhabditis elegans - physiology | Animals | Forkhead Transcription Factors - metabolism | Aging | Mice | Sirtuins - genetics | Caenorhabditis elegans Proteins - genetics | Sirtuins - metabolism | NAD - metabolism | Index Medicus
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3. Full Text Alkylating DNA damage stimulates a regulated form of necrotic cell death
by Zong, Wei-Xing and Ditsworth, Dara and Bauer, Daniel E and Wang, Zhao-Qi and Thompson, Craig B
Genes and Development, ISSN 0890-9369, 06/2004, Volume 18, Issue 11, pp. 1272 - 1282
Necrosis has been considered a passive form of cell death in which the cell dies as a result of a bioenergetic catastrophe imposed by external conditions.... 
Alkylating DNA damage | Bax | PARP | Metabolism | Bak | Necrosis | p53 | APOPTOSIS | POLY(ADP-RIBOSE) POLYMERASE GENE | DEVELOPMENTAL BIOLOGY | RELEASE | alkylating DNA damage | BCL-2 | CHROMATIN PROTEIN | MICE RESISTANT | necrosis | GLUCOSE-METABOLISM | DISEASE | GENETICS & HEREDITY | metabolism | ENDOPLASMIC-RETICULUM | Tumor Necrosis Factor-alpha - metabolism | Inflammation - pathology | Alkylating Agents - pharmacology | Molecular Sequence Data | Tumor Suppressor Protein p53 - genetics | Poly(ADP-ribose) Polymerases - drug effects | Inflammation - metabolism | DNA Damage - physiology | Mice, Mutant Strains | Adenosine Triphosphate - metabolism | Base Sequence | HMGB1 Protein - metabolism | Membrane Proteins - metabolism | NAD - metabolism | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - drug effects | Macrophages - pathology | Membrane Proteins - genetics | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Proto-Oncogene Proteins - genetics | bcl-2-Associated X Protein | Enzyme Activation - drug effects | Fibroblasts - pathology | Tumor Suppressor Protein p53 - drug effects | Macrophages - metabolism | Poly(ADP-ribose) Polymerases - metabolism | Animals | bcl-2 Homologous Antagonist-Killer Protein | Membrane Proteins - drug effects | Macrophages - drug effects | Mice | Proto-Oncogene Proteins c-bcl-2 | Proteins | Research | Cell death | DNA repair | DNA damage | Index Medicus | Research Papers
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4. Full Text Human Keratinocytes Express Functional Toll-Like Receptor 3, 4, 5, and 9
by Lebre, Maria C and van der Aar, Angelic M.G and van Baarsen, Lisa and van Capel, Toni M.M and Schuitemaker, Joost H.N and Kapsenberg, Martien L and de Jong, Esther C
Journal of Investigative Dermatology, ISSN 0022-202X, 02/2007, Volume 127, Issue 2, pp. 331 - 341
Keratinocytes are continuously in contact with external stimuli and have the capacity to produce several soluble mediators. Pathogen-associated molecular... 
TOLL-LIKE-RECEPTORS | DOUBLE-STRANDED-RNA | DENDRITIC CELLS | SKIN-ASSOCIATED CHEMOKINE | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | INNATE IMMUNE-RESPONSE | INFLAMMATORY PROTEIN 3-ALPHA | NECROSIS-FACTOR-ALPHA | FACTOR-KAPPA-B | HUMAN EPIDERMAL-KERATINOCYTES | DERMATOLOGY | Oligonucleotides - genetics | Phosphorylation | Toll-Like Receptor 5 - genetics | Humans | Toll-Like Receptor 9 - genetics | I-kappa B Proteins - metabolism | RNA, Messenger - metabolism | Flagellin - pharmacology | Tissue Distribution | Cell Nucleus - metabolism | Protein Isoforms - metabolism | Biological Transport | Oligonucleotides - pharmacology | Toll-Like Receptor 3 - genetics | Toll-Like Receptors - metabolism | Chemokine CXCL9 | Toll-Like Receptor 5 - metabolism | Poly I-C - pharmacology | Cytokines - metabolism | Cells, Cultured | Toll-Like Receptor 4 - genetics | Toll-Like Receptor 3 - metabolism | Toll-Like Receptor 4 - metabolism | Chemokine CXCL10 | Transcription Factor RelA - metabolism | Keratinocytes - metabolism | Toll-Like Receptors - genetics | Chemokines, CXC - metabolism | Lipopolysaccharides - pharmacology | CpG Islands | Ligands | Chemokines - metabolism | Toll-Like Receptor 9 - metabolism | CD40 antigen | Oligonucleotides | Flagellin | mRNA | intercellular adhesion molecule 1 | Immunity | Lipopolysaccharides | CXC chemokines | CCL20 protein | Toll-like receptors | CpG islands | TLR7 protein | Dermatology | Keratinocytes | Nuclear transport | Stress | TLR3 protein | TLR9 protein | TLR1 protein | External stimuli | CXCL10 protein | Histocompatibility antigen HLA | Interferon | Internet | Monocyte chemoattractant protein 1 | Tumor necrosis factor- alpha | Index Medicus
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5. Full Text Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation
by Haining Yang and Zeyana Rivera and Sandro Jube and Masaki Nasu and Pietro Bertino and Chandra Goparaju and Guido Franzoso and Michael T. Lotze and Thomas Krausz and Harvey I. Pass and Marco E. Bianchi and Michele Carbone and Janet D. Rowley
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2010, Volume 107, Issue 28, pp. 12611 - 12616
Asbestos carcinogenesis has been linked to the release of cytokines and mutagenic reactive oxygen species (ROS) from inflammatory cells. Asbestos is cytotoxic... 
Actinomycin | Asbestos | Cell death | Secretion | Plasma cells | Inflammation | Macrophages | Carcinogenesis | Necrosis | Apoptosis | Mesothelioma | Biomarker | Tumor necrosis factor-alpha | Chemoprevention | TRANSFORMATION | POLY(ADP-RIBOSE) POLYMERASE | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | CROCIDOLITE ASBESTOS | HMGB1 | biomarker | MAMMALIAN-CELLS | tumor necrosis factor-alpha | PATHOGENESIS | chemoprevention | NECROTIC CELLS | carcinogenesis | TNF-ALPHA | INHIBITORS | mesothelioma | Tumor Necrosis Factor-alpha - metabolism | Asbestos - metabolism | Epithelial Cells - metabolism | Reactive Oxygen Species - metabolism | Humans | Reactive Oxygen Species - pharmacology | Adenosine Diphosphate Ribose - metabolism | Adenosine Diphosphate Ribose - pharmacology | Carcinogens - metabolism | Asbestos - pharmacology | Pleural Neoplasms - metabolism | Inflammation - metabolism | Carcinogens - pharmacology | Cell Nucleus - metabolism | HMGB Proteins - pharmacology | HMGB1 Protein - pharmacology | HMGB1 Protein - metabolism | Cell Death | Mesocricetus | Female | HMGB Proteins - metabolism | Poly Adenosine Diphosphate Ribose - pharmacology | Epithelium - drug effects | Cricetinae | Cytokines - metabolism | Epithelium - metabolism | Hydrogen Peroxide - pharmacology | Necrosis - metabolism | Hydrogen Peroxide - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Macrophages - metabolism | Poly(ADP-ribose) Polymerases - metabolism | Animals | Mesothelioma - metabolism | Poly(ADP-ribose) Polymerases - pharmacology | Cells - metabolism | Mice | Mice, Inbred BALB C | Cytokines - pharmacology | Prevention | Mesothelium | Chromosomal proteins | Research | Chemical properties | Health aspects | Proteins | Carcinogens | Cytokines | Oncology | Biochemistry | Cells | Index Medicus | Reactive oxygen species | Transformation | Deposits | Hydrogen peroxide | Cytotoxicity | HMGB1 protein | Nuclei | Tumor necrosis factor-a | ATP | Cytoplasm | Biological Sciences
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6. Full Text Controlled Cell Adhesion on Poly(dopamine) Interfaces Photopatterned with Non‐Fouling Brushes
by Rodriguez‐Emmenegger, Cesar and Preuss, Corinna M and Yameen, Basit and Pop‐Georgievski, Ognen and Bachmann, Michael and Mueller, Jan O and Bruns, Michael and Goldmann, Anja S and Bastmeyer, Martin and Barner‐Kowollik, Christopher
Advanced Materials, ISSN 0935-9648, 11/2013, Volume 25, Issue 42, pp. 6123 - 6127
Bioinspired poly(dopamine) (PDA) films are merged with antifouling poly(MeOEGMA) brushes utilizing a nitrile imine‐mediated tetrazole‐ene cycloaddition... 
nitrile imine‐mediated tetrazole‐ene cycloaddition (NITEC) | micropatterning | photoligation | poly(dopamine) | antifouling polymer brushes | nitrile imine-mediated tetrazole-ene cycloaddition (NITEC) | PHYSICS, CONDENSED MATTER | PHYSICS, APPLIED | CLICK CHEMISTRY | BLOOD-PLASMA | MATERIALS SCIENCE, MULTIDISCIPLINARY | PROTEIN RESISTANCE | CHEMISTRY, PHYSICAL | NANOSCIENCE & NANOTECHNOLOGY | CHEMISTRY, MULTIDISCIPLINARY | FUNCTIONALIZATION | ION MASS-SPECTROMETRY | PHOTOCLICK CHEMISTRY | 1,3-DIPOLAR CYCLOADDITION | POLYMER BRUSHES | COATINGS | SURFACE-CHEMISTRY | Polyethylene Glycols - metabolism | Recombinant Fusion Proteins - biosynthesis | Cell Line | Green Fluorescent Proteins - metabolism | Cell Adhesion Molecules - genetics | Acrylates - chemistry | Rats | Polyethylene Glycols - chemistry | Green Fluorescent Proteins - genetics | Phosphoproteins - genetics | Phosphoproteins - metabolism | Cell Adhesion | Cell Adhesion Molecules - metabolism | Indoles - metabolism | Animals | Acrylates - metabolism | Recombinant Fusion Proteins - genetics | Polymers - chemistry | Microfilament Proteins - metabolism | Indoles - chemistry | Microfilament Proteins - genetics | Silicon - chemistry | Polymers - metabolism | Phenols | Polymers | Adhesion | Index Medicus
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7. Full Text Proteins with CHADs (Conserved Histidine alpha-Helical Domains) Are Attached to Polyphosphate Granules In Vivo and Constitute a Novel Family of Polyphosphate-Associated Proteins (Phosins)
by Tumlirsch, T and Jendrossek, D
APPLIED AND ENVIRONMENTAL MICROBIOLOGY, ISSN 0099-2240, 04/2017, Volume 83, Issue 7, p. E03399
On the basis of bioinformatic evidence, we suspected that proteins with a CYTH (CyaB thiamine triphosphatase) domain and/or a CHAD (conserved histidine... 
ACIDOCALCISOMES | INORGANIC POLYPHOSPHATE | volutin granules | MICROBIOLOGY | POLY(3-HYDROXYBUTYRATE) | polyphosphate | PHB GRANULES | Ralstonia eutropha | RALSTONIA-EUTROPHA H16 | polyhydroxyalkanoates (PHA) | GENOME SEQUENCE | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | Magnetospirillum gryphiswaldense | WASTE-WATER | biopolymers | ACCUMULATION | Pseudomonas putida | BIOLOGICAL PHOSPHORUS REMOVAL | PSEUDOMONAS-PUTIDA KT2440 | Protein Conformation, alpha-Helical | Magnetospirillum - metabolism | Bacterial Proteins - chemistry | Bacterial Proteins - genetics | Proteome | Histidine - metabolism | Biopolymers | Cupriavidus necator - genetics | Cupriavidus necator - metabolism | Polyphosphates - metabolism | Pseudomonas putida - metabolism | Bacterial Proteins - metabolism | Luminescent Proteins - genetics | Histidine - chemistry | Gram-Negative Aerobic Bacteria - metabolism | Polyphosphates - chemistry | Genetic aspects | Histidine | Research | Membrane proteins | Protein expression | Biochemistry | Gram-negative bacteria | Kinases | Bioinformatics | Proteomics | Index Medicus
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8. Full Text Prenatal Interaction of Mutant DISC1 and Immune Activation Produces Adult Psychopathology
by Abazyan, Bagrat|Nomura, Jun|Kannan, Geetha|Ishizuka, Koko|Tamashiro, Kellie L.|Nucifora, Frederick|Pogorelov, Vladimir|Ladenheim, Bruce|Yang, Chunxia|Krasnova, Irina N.|Cadet, Jean Lud|Pardo, Carlos|Mori, Susumu|Kamiya, Atsushi|Vogel, Michael W.|Sawa, Akira|Ross, Christopher A.|Pletnikov, Mikhail V
Biological Psychiatry, ISSN 0006-3223, 2010, Volume 68, Issue 12, pp. 1172 - 1181
Background Gene-environment interactions (GEI) are involved in the pathogenesis of mental diseases. We evaluated interaction between mutant human... 
Psychiatry | mouse models | Tet-off system | schizophrenia | DISC1 | gene-environment interactions | mood disorders | PSYCHIATRY | BEHAVIORAL PHENOTYPES | BIPOLAR DISORDER | NEUROSCIENCES | PREFRONTAL CORTEX | GENOMIC STRUCTURE | DENDRITIC SPINE DENSITY | INFECTION | SCHIZOPHRENIA RISK | INDUCIBLE EXPRESSION | Mood Disorders - genetics | Prenatal Exposure Delayed Effects - psychology | Microtubule-Associated Proteins - metabolism | Glycogen Synthase Kinase 3 beta | Male | Brain - metabolism | Mice, Mutant Strains | Stress, Psychological - metabolism | Atrophy - genetics | Behavior, Animal - drug effects | Female | Corticosterone - blood | Disease Models, Animal | Animals, Newborn | Poly I-C - pharmacology | Cytokine Receptor gp130 - metabolism | Cytokines - metabolism | Mice, Transgenic | Glycogen Synthase Kinase 3 - metabolism | Nerve Tissue Proteins - genetics | Prenatal Exposure Delayed Effects - metabolism | Pregnancy | Prenatal Exposure Delayed Effects - genetics | 1-Alkyl-2-acetylglycerophosphocholine Esterase - metabolism | Animals | Carrier Proteins - metabolism | Prenatal Exposure Delayed Effects - immunology | Mood Disorders - pathology | Dendritic Spines - pathology | Brain - pathology | Mice | Biogenic Monoamines - metabolism | GRB2 Adaptor Protein - metabolism | Atrophy - metabolism | Brain - immunology | Mood Disorders - metabolism | Psychological aspects | Schizophrenia | Neurosciences | Universities and colleges | Pregnant women | Analysis | Index Medicus
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9. Full Text Rapamycin treatment augments motor neuron degeneration in SOD1(G93A) mouse model of amyotrophic lateral sclerosis
by Zhang, XJ and Li, LA and Chen, S and Yang, DH and Wang, Y and Zhang, X and Wang, Z and Le, WD
AUTOPHAGY, ISSN 1554-8627, 04/2011, Volume 7, Issue 4, pp. 412 - 425
Aberrant protein misfolding may contribute to the pathogenesis of amyotrophic lateral sclerosis (ALS) but the detailed mechanisms are largely unknown. Our... 
LIFE-SPAN | autophagy | ALS | apoptosis | NEURODEGENERATION | CELL-DEATH | CELL BIOLOGY | MUTANT MICE | motor neuron degeneration | ROLES | protein aggregation | DEGRADATION | TRANSGENIC MICE | DISEASE PROGRESSION | Neurodegenerative Diseases - pathology | Spinal Cord - metabolism | TOR Serine-Threonine Kinases - metabolism | Sequestosome-1 Protein | Amyotrophic Lateral Sclerosis - genetics | Heat-Shock Proteins - metabolism | Caspase 3 - metabolism | bcl-2-Associated X Protein - metabolism | Mitochondria - metabolism | Autophagy | Sirolimus - pharmacology | Motor Neurons - pathology | Poly(ADP-ribose) Polymerases - metabolism | Animals | Superoxide Dismutase - physiology | Amyotrophic Lateral Sclerosis - metabolism | Mice | Superoxide Dismutase-1 | Adaptor Proteins, Signal Transducing - metabolism | Immunosuppressive Agents - pharmacology | Disease Models, Animal | Index Medicus
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10. Full Text Withaferin A induces p53-dependent apoptosis by repression of HPV oncogenes and upregulation of tumor suppressor proteins in human cervical cancer cells
by Munagala, Radha and Kausar, Hina and Munjal, Charu and Gupta, Ramesh C
Carcinogenesis, ISSN 0143-3334, 11/2011, Volume 32, Issue 11, pp. 1697 - 1705
Cervical cancer is caused by human papilloma virus (HPV) expressing E6 and E7 oncoproteins, which are known to inactivate tumor suppressor proteins p53 and... 
ACTIVATION | INHIBITION | CARCINOMA CELLS | ONCOLOGY | COMPOUND WITHAFERIN | DNA | IN-VIVO | STAT3 | CYCLE ARREST | DEPENDENT APOPTOSIS | P53 FUNCTION | Immunoprecipitation | Tumor Suppressor Protein p53 - antagonists & inhibitors | Apoptosis - drug effects | Humans | Papillomavirus E7 Proteins - antagonists & inhibitors | Uterine Cervical Neoplasms - pathology | Repressor Proteins - antagonists & inhibitors | Tumor Suppressor Protein p53 - genetics | Flow Cytometry | Oncogene Proteins, Viral - antagonists & inhibitors | Uterine Cervical Neoplasms - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Phosphorylation - drug effects | Tumor Cells, Cultured | Real-Time Polymerase Chain Reaction | Repressor Proteins - metabolism | Oncogene Proteins, Viral - metabolism | Tumor Suppressor Proteins - metabolism | RNA, Messenger - genetics | Tumor Suppressor Protein p53 - metabolism | Uterine Cervical Neoplasms - drug therapy | Blotting, Western | Papillomavirus E7 Proteins - metabolism | Animals | Withanolides - pharmacology | Mice, Nude | Cell Proliferation - drug effects | Mice | Cell Cycle - drug effects | Index Medicus
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11. Full Text Inhibition of phosphatidylinositol 3-kinase/AKT signaling by NVP-BKM120 promotes ABT-737-induced toxicity in a caspase-dependent manner through mitochondrial dysfunction and DNA damage response in established and primary cultured glioblastoma cells
by Jane, Esther P and Premkumar, Daniel R and Morales, Alejandro and Foster, Kimberly A and Pollack, Ian F
Journal of Pharmacology and Experimental Therapeutics, ISSN 0022-3565, 2014, Volume 350, Issue 1, pp. 22 - 35
Identification of therapeutic strategies that might enhance the efficacy of B-cell lymphoma-2 (Bcl-2) inhibitor ABT-737 [N-{4-[4(... 
MALIGNANT GLIOMA-CELLS | APOPTOSIS-INDUCING LIGAND | LYMPHOMA-CELLS | BAX ACTIVATION | SOLID TUMORS | MIMETIC ABT-737 TARGETS | BCL-2 FAMILY PROTEINS | PHARMACOLOGY & PHARMACY | MCL-1 DOWN-REGULATION | MEMBRANE PERMEABILIZATION | BRAIN-TUMORS | Glioblastoma - enzymology | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Humans | Caspase 3 - metabolism | Caspase 8 - metabolism | Piperazines - toxicity | Intracellular Signaling Peptides and Proteins - metabolism | Chromosome Segregation - drug effects | Membrane Potential, Mitochondrial - drug effects | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Biphenyl Compounds - toxicity | Proto-Oncogene Proteins c-bcl-2 - metabolism | Caspases - metabolism | Bcl-2-Like Protein 11 | Glioblastoma - genetics | Mitochondrial Proteins - metabolism | Glioblastoma - metabolism | Antineoplastic Agents - pharmacology | Proto-Oncogene Proteins | Cell Death - drug effects | Apoptosis Inducing Factor - metabolism | DNA Damage - drug effects | Cytochromes c - metabolism | bcl-2-Associated X Protein - metabolism | Morpholines - pharmacology | Mitochondria - metabolism | Mitochondria - drug effects | Mitochondria - pathology | Nitrophenols - toxicity | Drug Synergism | Membrane Proteins | Poly(ADP-ribose) Polymerases - metabolism | Apoptosis Regulatory Proteins | Signal Transduction - drug effects | Aminopyridines - pharmacology | Glioblastoma - pathology | Cell Line, Tumor | Sulfonamides - toxicity | Primary Cell Culture | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus | Cellular and Molecular
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12. Full Text Sirtuin 1-mediated cellular metabolic memory of high glucose via the LKB1/AMPK/ROS pathway and therapeutic effects of metformin
by Zheng, Zhi and Chen, Haibing and Li, Jun and Li, Tao and Zheng, Bingqing and Zheng, Ying and Jin, Huiyi and He, Ying and Gu, Qing and Xu, N
Diabetes, ISSN 0012-1797, 01/2012, Volume 61, Issue 1, pp. 217 - 228
Cellular metabolic memory occurs in diabetic microvascular and macrovascular complications, but the underlying mechanisms remain unclear. Here, we investigate... 
INTIMA-MEDIA THICKNESS | IN-VITRO | ACTIVATED PROTEIN-KINASE | OXYGEN SPECIES PATHWAY | INHIBITION | TYPE-1 DIABETES-MELLITUS | INSULIN-RESISTANCE | ENDOTHELIAL-CELLS | ENDOCRINOLOGY & METABOLISM | UP-REGULATION | HYPERGLYCEMIC DAMAGE | Retina - drug effects | Sirtuin 1 - metabolism | Gene Expression Regulation, Enzymologic - drug effects | Diabetes Mellitus, Experimental - drug therapy | Retina - metabolism | Metformin - therapeutic use | Reactive Oxygen Species - metabolism | Reactive Oxygen Species - pharmacology | NF-kappa B - metabolism | Sirtuin 1 - genetics | Diabetes Mellitus, Experimental - blood | Osmolar Concentration | Cattle | Adenylate Kinase - metabolism | Adenylate Kinase - physiology | Diabetes Mellitus, Experimental - metabolism | Endothelial Cells - physiology | Protein-Serine-Threonine Kinases - metabolism | Hypoglycemic Agents - therapeutic use | Endothelial Cells - metabolism | Protein-Serine-Threonine Kinases - physiology | Metformin - pharmacology | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Rats | Hypoglycemic Agents - pharmacology | Metabolic Networks and Pathways - genetics | Animals | Sirtuin 1 - physiology | Diabetes Mellitus, Experimental - pathology | Metabolic Networks and Pathways - drug effects | Blood Glucose - metabolism | Retina - pathology | Endothelial Cells - drug effects | Hyperglycemia | Physiological aspects | Development and progression | Research | Diabetes | Glucose | Adenylic acid | Dextrose | Sirtuins | Oxygen | Bax protein | Diabetes mellitus | Memory | Poly(ADP-ribose) polymerase | Retina | AMP-activated protein kinase | SIRT1 protein | Endothelial cells | Stress | LKB1 protein | Mitochondria | NF- Kappa B protein | Glyceraldehyde-3-phosphate dehydrogenase | Metformin | Apoptosis | Index Medicus | Abridged Index Medicus | Complications
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