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PLoS pathogens, ISSN 1553-7374, 2015, Volume 11, Issue 9, p. e1005142
Pharmacologically-induced activation of replication competent proviruses from latency in the presence of antiretroviral treatment (ART) has been proposed as a... 
ACTIVATION | RNA | PERSISTENCE | CD4(+) T-CELLS | MICROBIOLOGY | VIROLOGY | HISTONE DEACETYLASES | ACTIVE ANTIRETROVIRAL THERAPY | IMMUNODEFICIENCY-VIRUS TYPE-1 | STEM-CELL | INFECTION | PARASITOLOGY | VIRAL RESERVOIR | Follow-Up Studies | Humans | Middle Aged | Antiretroviral Therapy, Highly Active - adverse effects | Male | RNA, Viral - blood | AIDS Vaccines - therapeutic use | Virus Latency - drug effects | AIDS Vaccines - adverse effects | Anti-HIV Agents - administration & dosage | HIV Infections - immunology | Drug Interactions | HIV-1 - physiology | Lymphocytes - immunology | Protein Processing, Post-Translational - drug effects | HIV-1 - isolation & purification | Adult | Anti-HIV Agents - therapeutic use | Female | Depsipeptides - therapeutic use | RNA, Viral - metabolism | Depsipeptides - adverse effects | Biomarkers - metabolism | Lymphocytes - metabolism | HIV-1 - drug effects | Anti-HIV Agents - adverse effects | HIV Infections - virology | Biomarkers - blood | Histones - blood | Acetylation - drug effects | HIV-1 - immunology | Virus Activation - drug effects | Lymphocytes - drug effects | HIV Infections - drug therapy | Histones - metabolism | Infusions, Intravenous | Viral Load - drug effects | Cohort Studies | Depsipeptides - administration & dosage | HIV Infections - metabolism | Studies | Plasma | HIV | Acquired immune deficiency syndrome | Cytokines | Lymphocytes | Curing | AIDS | Infections | Human immunodeficiency virus | Research | Drug therapy
Journal Article
Nature (London), ISSN 1476-4687, 2012, Volume 487, Issue 7408, pp. 482 - 485
.... Here we isolated the circulating resting CD4(+) T cells of patients in whom viraemia was fully suppressed by antiretroviral therapy, and directly studied the effect of VOR on this latent reservoir... 
CELLS | ACTIVATION | SUBEROYLANILIDE HYDROXAMIC ACID | MULTIDISCIPLINARY SCIENCES | IN-VIVO | VALPROIC ACID | INFECTION | HISTONE DEACETYLASE INHIBITORS | TYPE-1 | EXPRESSION | PCR | Gene Expression Regulation, Viral - drug effects | Humans | Hydroxamic Acids - adverse effects | Histone Deacetylase Inhibitors - administration & dosage | RNA, Viral - blood | Virus Latency - drug effects | Proviruses - drug effects | HIV-1 - growth & development | Proviruses - genetics | Hydroxamic Acids - administration & dosage | Anti-HIV Agents - therapeutic use | CD4-Positive T-Lymphocytes - virology | Hydroxamic Acids - pharmacology | Biomarkers - metabolism | HIV Infections - blood | Risk Assessment | HIV-1 - drug effects | CD4-Positive T-Lymphocytes - cytology | HIV Infections - virology | RNA, Viral - biosynthesis | CD4-Positive T-Lymphocytes - metabolism | Viremia - drug therapy | HIV-1 - genetics | Proviruses - growth & development | Histones - drug effects | Up-Regulation - drug effects | Acetylation - drug effects | Viremia - virology | HIV Infections - drug therapy | Histone Deacetylase Inhibitors - pharmacology | Histones - metabolism | CD4-Positive T-Lymphocytes - drug effects | Histone Deacetylase Inhibitors - adverse effects | Physiological aspects | Antiviral agents | HIV patients | Health aspects | Vorinostat | Antiretroviral drugs | Plasma | Cell culture | Lymphocytes | Human immunodeficiency virus--HIV | Genomes | Drug therapy | Drug dosages
Journal Article
Autophagy, ISSN 1554-8627, 05/2012, Volume 8, Issue 5, pp. 812 - 825
.... Furthermore, our results revealed that curcumin causes some novel cellular mechanisms that promote autophagy as a protective effect... 
autophagy | endothelial cell | FOXO1 | oxidative stress | curcumin | Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Oxidative stress | Endothelial cell | Curcumin | Autophagy | TOR Serine-Threonine Kinases - metabolism | Apoptosis - drug effects | Humans | Phosphatidylinositol 3-Kinases - metabolism | Protein Transport - drug effects | Autophagy - drug effects | Gene Knockdown Techniques | Proto-Oncogene Proteins c-bcl-2 - metabolism | Cell Nucleus - metabolism | Forkhead Transcription Factors - metabolism | Protective Agents - pharmacology | Protein Binding - drug effects | Cytoprotection - drug effects | Membrane Proteins - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Beclin-1 | Hydrogen Peroxide - toxicity | rab GTP-Binding Proteins - metabolism | Cell Survival - drug effects | Human Umbilical Vein Endothelial Cells - drug effects | Curcumin - pharmacology | Down-Regulation - drug effects | Ubiquitin-Activating Enzymes - metabolism | Apoptosis Regulatory Proteins - metabolism | Up-Regulation - drug effects | Acetylation - drug effects | Autophagy-Related Protein 7 | Human Umbilical Vein Endothelial Cells - enzymology | Signal Transduction - drug effects | Models, Biological | Human Umbilical Vein Endothelial Cells - pathology | Forkhead Box Protein O1 | Oxidative Stress - drug effects | Cell Nucleus - drug effects | CELL BIOLOGY
Journal Article
Biomaterials, ISSN 0142-9612, 2015, Volume 67, pp. 169 - 182
.... Ac-aCD NP was able to dramatically potentiate the activity of anticancer drugs including paclitaxel, docetaxel, cis-diamminedichloroplatinum, camptothecin, and doxorubicin... 
Advanced Basic Science | Dentistry | Cyclodextrin | Drug delivery | Pgp inhibitor | Nanomedicine | Multidrug resistance | pH-responsive | PH-responsive | MATERIALS SCIENCE, BIOMATERIALS | ATPASE ACTIVITY | ENGINEERING, BIOMEDICAL | DIMETHYL-BETA-CYCLODEXTRIN | DOXORUBICIN | NANOCARRIERS | PLURONIC BLOCK-COPOLYMERS | BLOOD-BRAIN-BARRIER | DELIVERY | NANOPARTICLES | GLYCOPROTEIN | NANOTECHNOLOGY | Doxorubicin - therapeutic use | Paclitaxel - pharmacology | Nanoparticles - chemistry | Apoptosis - drug effects | Drug Resistance, Multiple - drug effects | Humans | ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism | alpha-Cyclodextrins - chemistry | Antineoplastic Agents - therapeutic use | Membrane Potential, Mitochondrial - drug effects | Antineoplastic Agents - pharmacology | Cell Membrane - metabolism | Acetylation | Cell Membrane - drug effects | Endocytosis - drug effects | Nanoparticles - ultrastructure | Adenosine Triphosphatases - metabolism | Nanoparticles - toxicity | Paclitaxel - therapeutic use | Neoplasms - drug therapy | Rhodamine 123 - metabolism | Cell Line, Tumor | Cytoskeleton - metabolism | Cell Cycle - drug effects | Neoplasms - pathology | Cytoskeleton - drug effects | Doxorubicin - pharmacology | Energy Metabolism - drug effects | Drug Resistance, Neoplasm - drug effects | Hydrogen-Ion Concentration | Drugs | Drug resistance in microorganisms | Medical colleges | Anthracyclines | Drugstores | Cyclodextrins | Hydrolysis | Chemotherapy | Pharmacy | Cancer cells | Drug therapy | Hydrogen-ion concentration | Adenosine triphosphatase | Cancer | Drug delivery systems | Vehicles | Demand | Membranes | Reversion | Nanostructure
Journal Article
International journal of cancer, ISSN 0020-7136, 08/2008, Volume 123, Issue 3, pp. 552 - 560
Genistein is a phytoestrogen that has been reported to suppress the AKT signaling pathway in several malignancies. However, the molecular mechanism of... 
Prostate cancer | Genistein | Tumor suppressor gene | APOPTOSIS | METHYLATION | PROTEIN-KINASE | TRANSCRIPTION | SIRT1 | FACULTATIVE HETEROCHROMATIN | CYLD | prostate cancer | genistein | ONCOLOGY | SIGNALING PATHWAY | NF-KAPPA-B | EXPRESSION | tumor suppressor gene | PTEN Phosphohydrolase - drug effects | Prostatic Neoplasms - metabolism | Deubiquitinating Enzyme CYLD | CpG Islands - drug effects | Humans | Male | NF-kappa B - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Genes, Tumor Suppressor - drug effects | Genes, p53 - drug effects | Prostatic Neoplasms - genetics | Chromatin Immunoprecipitation | Forkhead Transcription Factors - metabolism | Sirtuin 1 | Antimetabolites, Antineoplastic - pharmacology | Electrophoretic Mobility Shift Assay | Gene Expression Regulation, Neoplastic - drug effects | Chromones - pharmacology | Anticarcinogenic Agents - pharmacology | Hydroxamic Acids - pharmacology | Phytoestrogens - pharmacology | Prostatic Neoplasms - drug therapy | PTEN Phosphohydrolase - genetics | Tumor Suppressor Proteins - metabolism | Enzyme Inhibitors - pharmacology | Morpholines - pharmacology | PTEN Phosphohydrolase - metabolism | Azacitidine - analogs & derivatives | Down-Regulation - drug effects | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Histones - drug effects | Gene Expression Regulation - drug effects | Up-Regulation - drug effects | Azacitidine - pharmacology | Acetylation - drug effects | Methylation - drug effects | Genistein - pharmacology | Cell Line, Tumor | Protein Kinase Inhibitors - pharmacology | Histones - metabolism | Forkhead Box Protein O3 | Sirtuins - metabolism | NF-kappa B - drug effects | Index Medicus
Journal Article
Nature (London), ISSN 0028-0836, 03/2012, Volume 483, Issue 7388, pp. 222 - 226
Cognitive decline is a debilitating feature of most neurodegenerative diseases of the central nervous system, including Alzheimer's disease(1). The causes... 
REMOTE MEMORIES | LONG-TERM-MEMORY | CDK5 | CHROMATIN | PHOSPHORYLATION | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | CLINICAL-IMPLICATIONS | SYNAPTIC PLASTICITY | EXPRESSION | TRANSGENIC MICE | Memory Disorders - physiopathology | Alzheimer Disease - complications | Memory Disorders - genetics | Peptide Fragments - toxicity | Humans | Neuronal Plasticity - drug effects | Receptors, Glucocorticoid - metabolism | Hippocampus - drug effects | RNA Polymerase II - metabolism | Memory Disorders - complications | Promoter Regions, Genetic - drug effects | Promoter Regions, Genetic - genetics | Gene Knockdown Techniques | Brain - metabolism | Neuronal Plasticity - genetics | Epigenesis, Genetic - drug effects | Phosphorylation - drug effects | Disease Models, Animal | Hydrogen Peroxide - toxicity | Histone Deacetylase 2 - genetics | Alzheimer Disease - physiopathology | Amyloid beta-Peptides - toxicity | Brain - physiopathology | Neurodegenerative Diseases - genetics | Neurodegenerative Diseases - complications | Brain - drug effects | Gene Expression Regulation - drug effects | Hippocampus - metabolism | Acetylation - drug effects | Animals | Neurodegenerative Diseases - physiopathology | Histone Deacetylase 2 - deficiency | Mice | Histone Deacetylase 2 - metabolism | Histones - metabolism | Alzheimer Disease - genetics | Epigenetic inheritance | Complications and side effects | Causes of | Nervous system | Genetic aspects | Degeneration | Cognition disorders | Health aspects | Epigenetics | Genetics | RNA polymerase | Kinases | Neurodegeneration | Cyclin-dependent kinases
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 1, p. e54001
Background: Histone deacetylase (HDAC) inhibitors are promising anti-fibrosis drugs... 
GROWTH-FACTOR-BETA | SOLID TUMORS | OBSTRUCTIVE NEPHROPATHY | MULTIDISCIPLINARY SCIENCES | CARDIAC-HYPERTROPHY | INTERSTITIAL FIBROSIS | INJURY | ANGIOTENSIN-II | CHRONIC KIDNEY-DISEASE | FACTOR RECEPTOR | MOLECULAR-MECHANISMS | Kidney - pathology | Transforming Growth Factor beta1 - metabolism | Actins - metabolism | Smad3 Protein - metabolism | Ureteral Obstruction - metabolism | Leukocytes - immunology | Kidney - metabolism | Receptor, Epidermal Growth Factor - metabolism | Benzamides - therapeutic use | Benzamides - pharmacology | Phosphorylation - drug effects | Ureteral Obstruction - drug therapy | Protein-Serine-Threonine Kinases - metabolism | Transforming Growth Factor beta1 - biosynthesis | Fibroblasts - metabolism | Pyridines - therapeutic use | Collagen Type I - metabolism | Kidney - drug effects | Histone Deacetylases - metabolism | Fibroblasts - pathology | Fibronectins - metabolism | Ureteral Obstruction - immunology | Gene Expression Regulation - drug effects | Acetylation - drug effects | Animals | Receptors, Transforming Growth Factor beta - metabolism | Signal Transduction - drug effects | Cell Cycle Checkpoints - drug effects | Fibroblasts - drug effects | Ureteral Obstruction - pathology | Fibrosis | Histone Deacetylase Inhibitors - pharmacology | Leukocytes - drug effects | Cell Proliferation - drug effects | Histone Deacetylase Inhibitors - therapeutic use | Mice | Pyridines - pharmacology | Histones - metabolism | Fibronectins | Muscle proteins | Growth factors | Collagen | Analysis | Drugs | Histone deacetylase | Phosphorylation | Smad protein | Animal models | Collagen (type I) | Nephrology | Transcription | Syngeneic grafts | Transforming growth factor-b | Smooth muscle | Activation | Kinases | Fibronectin | Medical schools | Epidermal growth factor | Actin | Rodents | Cell cycle | Fibroblasts | Ureter | Inhibition | Kidneys | Transforming growth factor-b1 | Epidermal growth factor receptors | Pulmonary arteries | Fibrils | Muscles | Medicine | Signaling | Hospitals | Kidney diseases | Cancer
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 4, p. e61807
The Notch pathway can have both oncogenic and tumor suppressor roles, depending on cell context. For example, Notch signaling promotes T cell differentiation... 
PROMOTER DNA METHYLATION | LYMPHOMAS | TUMOR-SUPPRESSOR FUNCTION | MULTIDISCIPLINARY SCIENCES | ACUTE LYMPHOCYTIC-LEUKEMIA | GROWTH | GENES | TRANSCRIPTION | MALIGNANCIES | CANCER | TUMORIGENESIS | Transcription, Genetic - drug effects | Apoptosis - drug effects | Receptors, Notch - metabolism | Humans | Apoptosis - genetics | Receptors, Notch - genetics | Gene Expression Profiling | Hematopoiesis - drug effects | Basic Helix-Loop-Helix Transcription Factors - metabolism | T-Lymphocytes - metabolism | Serrate-Jagged Proteins | T-Lymphocytes - drug effects | B-Lymphocytes - pathology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - blood | B-Lymphocytes - metabolism | Repressor Proteins - metabolism | Bone Marrow - drug effects | Jagged-1 Protein | Basic Helix-Loop-Helix Transcription Factors - genetics | Membrane Proteins - genetics | Gene Expression Regulation, Leukemic - drug effects | Leukemia, B-Cell - pathology | Repressor Proteins - genetics | Hematopoiesis - genetics | Signal Transduction - genetics | Azacitidine - pharmacology | Leukemia, B-Cell - blood | Leukemia, B-Cell - genetics | Signal Transduction - drug effects | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics | Cell Line, Tumor | Histones - metabolism | DNA Methylation - drug effects | Calcium-Binding Proteins - genetics | Gene Silencing - drug effects | Blood Cells - metabolism | Cell Lineage - drug effects | Intercellular Signaling Peptides and Proteins - metabolism | Epigenesis, Genetic - drug effects | Membrane Proteins - metabolism | T-Lymphocytes - pathology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology | Blood Cells - drug effects | Hydroxamic Acids - pharmacology | Cell Lineage - genetics | Calcium-Binding Proteins - metabolism | Intercellular Signaling Peptides and Proteins - genetics | Azacitidine - analogs & derivatives | DNA Methylation - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | B-Lymphocytes - drug effects | Bone Marrow - pathology | Receptor, Notch3 | Cell Proliferation - drug effects | Sulfites | Epigenetic inheritance | DNA microarrays | Genes | Genetic aspects | Genetic engineering | Acute lymphocytic leukemia | B cells | T cells | Methylation | Cell differentiation | Biotechnology | Transcription factors | Bisulfite | Pathogenesis | Leukemia | Differentiation (biology) | Lymphocytes T | Kinases | Inactivation | Signal transduction | Restoration | Lymphocytes | DNA methylation | Bone marrow | Tumorigenesis | Acetylation | Deoxyribonucleic acid--DNA | CpG islands | Acute lymphatic leukemia | Deactivation | Lymphatic leukemia | Tumor cell lines | Gene silencing | Signaling | Lymphocytes B | Regulatory mechanisms (biology) | Stem cells | Epigenetics | Ligands | Tumor suppressor genes | Leukemogenesis | Lymphomas | Notch protein | Aberration | Apoptosis | Cancer | Deoxyribonucleic acid | DNA
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 7, p. e69964
... States of America Hank La Affiliation: Department of Drug Metabolism and Pharmacokinetics, Genentech, Inc., South San Francisco, California, United States of America... 
HIPPOCAMPUS | FEAR | MEMORY FORMATION | SUBEROYLANILIDE HYDROXAMIC ACID | ACETYLATION | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | MICE | HISTONE DEACETYLASE INHIBITORS | VORINOSTAT | ATP Binding Cassette Transporter, Sub-Family G, Member 2 | Humans | ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism | Brain - enzymology | Fear - drug effects | Neuronal Plasticity - drug effects | Excitatory Postsynaptic Potentials - drug effects | Membranes - drug effects | CA1 Region, Hippocampal - drug effects | Brain - metabolism | Long-Term Potentiation - drug effects | Isoenzymes - metabolism | ATP-Binding Cassette Transporters - metabolism | Hydroxamic Acids - administration & dosage | Inhibitory Concentration 50 | Behavior, Animal - drug effects | Hydroxamic Acids - pharmacology | Synapses - drug effects | CA1 Region, Hippocampal - physiology | Conditioning (Psychology) - drug effects | Synapses - physiology | Mice, Inbred C57BL | Rats | Histone Deacetylases - metabolism | Mice, Transgenic | Cognition - drug effects | Rats, Sprague-Dawley | Hydroxamic Acids - pharmacokinetics | Brain - drug effects | Phenotype | Animals | Mice | Neurons | Cognition | Non-Hodgkin's lymphomas | T cells | Alzheimer's disease | Neurophysiology | Potentiation | Brain | Histone deacetylase | Neurosciences | Chromatin | Disease | Synaptic strength | Memory | Brain slice preparation | Central nervous system | Immunological synapses | Experiments | Impact analysis | Behavioral plasticity | Blood-brain barrier | Acquired immune deficiency syndrome--AIDS | Neurodegeneration | Rodents | Synaptic plasticity | Synaptic depression | Excitation | Long-term depression | Availability | Efflux | Neurodegenerative diseases | Long-term potentiation | Hydroxamic acid | Excitability | Pharmacology | Metabolism | Gene expression | Lymphoma | Substrates | Acids | In vivo methods and tests | Laboratory animals | Synapses | Hippocampus | T-cell lymphoma | Animal cognition | Acquired immune deficiency syndrome | AIDS
Journal Article
Journal of endodontics, ISSN 0099-2399, 2012, Volume 38, Issue 3, pp. 339 - 345
Journal Article