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Developmental Cell, ISSN 1534-5807, 10/2016, Volume 39, Issue 1, pp. 13 - 27
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2017, Volume 12, Issue 4, pp. e0173676 - e0173676
Autophagy is a catabolic mechanism to degrade cellular components to maintain cellular energy levels during starvation, a condition where PPAR alpha may be... 
INSULIN SIGNALING TRANSDUCTION | GLUCOSE-HOMEOSTASIS | FIBROBLAST-GROWTH-FACTOR-21 | DEACETYLATION | METABOLISM | PATHWAY | STEATOSIS | MULTIDISCIPLINARY SCIENCES | RESISTANCE | RECEPTORS | FOXO1 | TOR Serine-Threonine Kinases - metabolism | Autophagy-Related Protein 7 - metabolism | Fibroblast Growth Factors - genetics | Autophagy-Related Protein 5 - genetics | fas Receptor - metabolism | Autophagy - drug effects | Fibroblast Growth Factors - metabolism | TOR Serine-Threonine Kinases - genetics | Liver - drug effects | fas Receptor - genetics | Autophagy - genetics | Proto-Oncogene Proteins c-akt - metabolism | Forkhead Box Protein O1 - metabolism | Signal Transduction | Liver - metabolism | PPAR alpha - genetics | Ubiquitin-Conjugating Enzymes - genetics | Stearoyl-CoA Desaturase - genetics | Mice, Knockout | Triglycerides - metabolism | Sequestosome-1 Protein - genetics | Ubiquitin-Conjugating Enzymes - metabolism | Cysteine Endopeptidases - genetics | Autophagy-Related Protein 5 - metabolism | Beclin-1 - genetics | Stearoyl-CoA Desaturase - metabolism | Mice | PPAR alpha - metabolism | Autophagy-Related Proteins - antagonists & inhibitors | Blood Glucose - metabolism | Autophagy-Related Proteins - metabolism | Forkhead Box Protein O1 - genetics | Autophagy-Related Protein 5 - antagonists & inhibitors | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Proto-Oncogene Proteins c-akt - genetics | Fenofibrate - pharmacology | Cysteine Endopeptidases - metabolism | Autophagy-Related Proteins - genetics | Sequestosome-1 Protein - metabolism | Sterol Regulatory Element Binding Protein 1 - metabolism | Autophagy-Related Protein 7 - antagonists & inhibitors | Mice, Inbred C57BL | Autophagy-Related Protein 7 - genetics | Gene Expression Regulation - drug effects | Animals | Sterol Regulatory Element Binding Protein 1 - genetics | PPAR alpha - agonists | Ubiquitin-Conjugating Enzymes - antagonists & inhibitors | Beclin-1 - metabolism | Transcription factors | Adipose tissue | Liver | Body weight | AKT protein | Biochemistry | Glucose | Assaying | Proteins | Signal transduction | Temperature effects | Fibroblasts | Physiology | Acetylation | Inhibition | Growth factors | Hepatotoxicity | Activation analysis | Methanol | Starvation | Ethanol | AMP | Metabolism | Insulin | Fatty acids | Studies | Acetaminophen | Food intake | Weight reduction | Animal welfare | Circulation | Drugs | Biotechnology | Drug abuse | Laboratories | Centrifugation | Glass | Homeostasis | Activation | Biology | Kinases | AMP-activated protein kinase | Autophagy | Nutrient status | Rodents | Nutrients | Oxidation | Heart diseases | Age | Epinephrine | AKT1 protein | Fasting | Chloroform | Diabetes mellitus | Cardiomyocytes | Acclimatization | Triglycerides | Pharmacology | Nitrogen | Calories | Medicine | Nuclear fuels | Protein kinase | Insulin resistance | Diabetes | Index Medicus
Journal Article
Molecular Cell, ISSN 1097-2765, 07/2011, Volume 43, Issue 1, pp. 19 - 32
Journal Article
Nature Cell Biology, ISSN 1465-7392, 09/2010, Volume 12, Issue 9, pp. 863 - 875
Accumulation of unwanted/misfolded proteins in aggregates has been observed in airways of patients with cystic fibrosis (CF), a life-threatening genetic... 
APOPTOSIS | UNFOLDED PROTEIN RESPONSE | BECLIN 1 | DOWN-REGULATION | ENDOPLASMIC-RETICULUM | MICE | GENE-TRANSFER | TISSUE TRANSGLUTAMINASE | NEURODEGENERATIVE DISEASES | CELL-DEATH | CELL BIOLOGY | Reactive Oxygen Species - metabolism | Respiratory Mucosa - drug effects | Sequestosome-1 Protein | Humans | Transglutaminases - genetics | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Autophagy - drug effects | Young Adult | Cystamine - therapeutic use | Inflammation - metabolism | Autophagy - genetics | Nasal Polyps - metabolism | Mice, Inbred CFTR | Respiratory Mucosa - cytology | Cystic Fibrosis - metabolism | Membrane Proteins - genetics | Mice, Transgenic | Protein Transport - genetics | Apoptosis Regulatory Proteins - metabolism | Reactive Oxygen Species - antagonists & inhibitors | Models, Biological | Cystic Fibrosis - genetics | Transglutaminases - metabolism | Adolescent | Cystic Fibrosis Transmembrane Conductance Regulator - genetics | Mice | GTP-Binding Proteins | Cystic Fibrosis - drug therapy | Protein Binding - physiology | Microtubule-Associated Proteins - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Salicylates - pharmacology | Epithelial Sodium Channels - genetics | Apoptosis Regulatory Proteins - genetics | Adult | Cystamine - pharmacology | Membrane Proteins - metabolism | Acetylcysteine - therapeutic use | Beclin-1 | Cystic Fibrosis Transmembrane Conductance Regulator - antagonists & inhibitors | Cell Line | Small Ubiquitin-Related Modifier Proteins - metabolism | Heat-Shock Proteins - metabolism | Cystic Fibrosis Transmembrane Conductance Regulator - metabolism | Antioxidants - pharmacology | Mice, Inbred Strains | Nasal Polyps - drug therapy | Antioxidants - therapeutic use | Animals | Acetylcysteine - pharmacology | Adaptor Proteins, Signal Transducing - genetics | Respiratory Mucosa - metabolism | Adaptor Proteins, Signal Transducing - metabolism | Organometallic Compounds - pharmacology | Complications and side effects | Active oxygen | Gene mutations | Lung diseases | Physiological aspects | Cystic fibrosis | Genetic aspects | Research | Health aspects | Risk factors | Index Medicus
Journal Article
Blood, ISSN 0006-4971, 02/2012, Volume 119, Issue 6, pp. 1490 - 1500
Ataxia-telangiectasia mutated (ATM) plays a central role in DNA damage responses, and its loss leads to development of T-cell malignancies. Here, we show that... 
OXIDATIVE STRESS | AUTOPHAGY GENE | BECLIN-1 | HEMATOPOIETIC STEM-CELLS | TUMOR-SUPPRESSOR | DJ-1 | IONIZING-RADIATION | HEMATOLOGY | CANCER | ATM-DEFICIENT MICE | PARKINSONS-DISEASE | Reactive Oxygen Species - metabolism | Thymocytes - metabolism | Humans | Immunoblotting | Autophagy | Lymphoma, T-Cell - metabolism | DNA-Binding Proteins - metabolism | Mitochondria - genetics | RNA Interference | Adenosine Triphosphate - metabolism | Tumor Suppressor Proteins - genetics | Membrane Potential, Mitochondrial | Apoptosis Regulatory Proteins - genetics | Cell Cycle Proteins - genetics | Membrane Proteins - metabolism | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Ataxia Telangiectasia - physiopathology | Beclin-1 | Microscopy, Electron, Transmission | Thymocytes - ultrastructure | Gene Expression | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Cells, Cultured | Kaplan-Meier Estimate | Oxygen Consumption | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia - metabolism | Mitochondria - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Lymphoma, T-Cell - genetics | Reverse Transcriptase Polymerase Chain Reaction | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Ataxia Telangiectasia - genetics | Fibroblasts - cytology | Mice | Mitochondria - physiology | Index Medicus | Abridged Index Medicus | Lymphoid Neoplasia
Journal Article
Nature Cell Biology, ISSN 1465-7392, 07/2013, Volume 15, Issue 7, pp. 741 - 750
Journal Article
The Journal of Physiology, ISSN 0022-3751, 10/2014, Volume 592, Issue 20, pp. 4575 - 4589
Prolonged skeletal muscle inactivity causes muscle fibre atrophy. Redox imbalance has been considered one of the major triggers of skeletal muscle disuse... 
TIBIALIS ANTERIOR | SKELETAL-MUSCLE | GAMMA COACTIVATOR 1-ALPHA | OXIDATIVE STRESS | PHYSIOLOGY | MITOCHONDRIAL BIOGENESIS | GENE-EXPRESSION | TRANSCRIPTIONAL COACTIVATOR | UBIQUITIN LIGASES | PROTEIN-SYNTHESIS | NEUROSCIENCES | ANTIOXIDANT CAPACITY | Up-Regulation | Dynamins - metabolism | Superoxide Dismutase - genetics | Oxidative Stress | SKP Cullin F-Box Protein Ligases - genetics | Mitochondria, Muscle - metabolism | Male | Muscle Fibers, Skeletal - drug effects | Muscle Fibers, Skeletal - metabolism | RNA, Messenger - metabolism | Autophagy | Tripartite Motif Proteins | Chromans - pharmacology | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Muscle Proteins - metabolism | Apoptosis Regulatory Proteins - genetics | NF-E2-Related Factor 2 - genetics | Muscular Atrophy - prevention & control | Muscle Fibers, Skeletal - physiology | Superoxide Dismutase - metabolism | Beclin-1 | Muscular Atrophy - metabolism | Catalase - genetics | Mice, Inbred C57BL | RNA, Messenger - genetics | Ubiquitin-Protein Ligases - metabolism | Dynamins - genetics | SKP Cullin F-Box Protein Ligases - metabolism | Antioxidants - pharmacology | Transcription Factors - genetics | Apoptosis Regulatory Proteins - metabolism | Catalase - metabolism | Muscle Proteins - genetics | Transcription Factors - metabolism | Antioxidants - therapeutic use | Animals | Chromans - therapeutic use | Hindlimb Suspension - adverse effects | NF-E2-Related Factor 2 - metabolism | Mice | Mitochondria, Muscle - drug effects | Superoxide Dismutase-1 | Ubiquitin-Protein Ligases - genetics | Index Medicus | Muscle
Journal Article
Scientific Reports, ISSN 2045-2322, 2013, Volume 3, Issue 1, pp. 1077 - 1077
Our studies in HUVECs show that ox-LDL induced autophagy and damaged mtDNA leading to TLR9 expression. LOX-1 antibody or the ROS inhibitor apocynin attenuated... 
HEART | APOPTOSIS | ATHEROGENESIS | ARTERY ENDOTHELIAL-CELLS | MULTIDISCIPLINARY SCIENCES | RECEPTOR | DEGRADATION | OXIDIZED-LDL | LOX-1 | Human Umbilical Vein Endothelial Cells | Leukocyte Common Antigens - metabolism | Reactive Oxygen Species - metabolism | Microtubule-Associated Proteins - metabolism | Humans | Toll-Like Receptor 9 - genetics | Autophagy - drug effects | Antigens, CD - metabolism | Inflammation - metabolism | RNA Interference | Diet, High-Fat | Endodeoxyribonucleases - metabolism | Receptors, LDL - deficiency | Beclin-1 | DNA Damage - drug effects | Receptors, LDL - genetics | Atherosclerosis - pathology | Endodeoxyribonucleases - antagonists & inhibitors | Scavenger Receptors, Class E - genetics | DNA, Mitochondrial - metabolism | Cells, Cultured | Lipoproteins, LDL - pharmacology | Receptors, LDL - metabolism | Atherosclerosis - metabolism | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Scavenger Receptors, Class E - metabolism | Endodeoxyribonucleases - genetics | Animals | Antigens, Differentiation, Myelomonocytic - metabolism | Mice | Oxidative Stress - drug effects | Scavenger Receptors, Class E - deficiency | Toll-Like Receptor 9 - metabolism | RNA, Small Interfering - metabolism | Lipoproteins (low density) | Deoxyribonuclease | Oxidative stress | Reactive oxygen species | High cholesterol diet | DNA damage | siRNA | Mitochondrial DNA | Inflammation | LOX-1 protein | Autophagy | TLR9 protein | Cholesterol | CD45 antigen | Clonal deletion | Arteriosclerosis | Rodents | Atherosclerosis | Toll-like receptors | Lipoprotein (low density) receptors | Phagocytosis | Index Medicus
Journal Article
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 06/2017, Volume 312, Issue 6, pp. F1128 - F1140
Chronic kidney disease (CKD) causes loss of lean body mass by multiple mechanisms. This study examines whether autophagy-mediated proteolysis contributes to... 
Acidification | FoxO | LC3II | Forkhead transcription factors | Overloading | Ubiquitin-proteasome system | CELLS | PHYSIOLOGY | ATROPHY | TRANSCRIPTION | acidification | PROTEOLYSIS | CATABOLIC CONDITIONS | ubiquitin-proteasome system | overloading | PROTEIN-DEGRADATION | DNA | IN-VIVO | UROLOGY & NEPHROLOGY | forkhead transcription factors | CKD | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Mitochondria, Muscle - metabolism | Male | Muscle, Skeletal - metabolism | Mitochondrial Proteins - genetics | Muscle Fibers, Skeletal - metabolism | Renal Insufficiency, Chronic - complications | RNA, Messenger - metabolism | Autophagy | DNA-Binding Proteins - metabolism | Organelle Biogenesis | Mitochondrial Proteins - metabolism | Adenosine Triphosphate - metabolism | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism | Membrane Proteins - metabolism | Muscular Atrophy - etiology | Disease Models, Animal | Cell Line | High Mobility Group Proteins - metabolism | Muscular Atrophy - metabolism | Membrane Proteins - genetics | Mitochondria, Muscle - pathology | Mice, Inbred C57BL | Muscular Atrophy - pathology | RNA, Messenger - genetics | Gene Expression Regulation | Muscular Atrophy - genetics | DNA-Binding Proteins - genetics | Renal Insufficiency, Chronic - blood | Animals | GTP Phosphohydrolases - metabolism | GTP Phosphohydrolases - genetics | Uremia - blood | Muscle Fibers, Skeletal - pathology | Beclin-1 - genetics | Mice | Muscle, Skeletal - pathology | Beclin-1 - metabolism | High Mobility Group Proteins - genetics | Proteins | Muscles | Acupuncture | Chronic kidney failure | Proteolysis | Myosin | Myotubes | Syngeneic grafts | Copy number | Satellite cells | BNIP3 protein | Skeletal muscle | Electrical stimuli | Musculoskeletal system | Mitochondria | Exercise | Body mass | Actin | Rodents | Lean body mass | Kidney diseases | Phagocytosis | Index Medicus
Journal Article
Molecular Biology of the Cell, ISSN 1059-1524, 12/2008, Volume 19, Issue 12, pp. 5360 - 5372
Class III phosphatidylinositol 3-kinase (PI3-kinase) regulates multiple membrane trafficking. In yeast, two distinct PI3-kinase complexes are known: complex I... 
PRE-AUTOPHAGOSOMAL STRUCTURE | LATE ENDOSOMES | MOLECULAR MACHINERY | PROTEIN-KINASE | TRANS-GOLGI NETWORK | TUMOR-SUPPRESSOR | VPS34 PTDINS 3-KINASE | SACCHAROMYCES-CEREVISIAE | SELECTIVE AUTOPHAGY | SELF-DIGESTION | CELL BIOLOGY | Autophagy-Related Proteins | Adaptor Proteins, Vesicular Transport - classification | Humans | Adaptor Proteins, Vesicular Transport - genetics | Molecular Sequence Data | rab GTP-Binding Proteins - genetics | Autophagy - physiology | Phosphatidylinositol 3-Kinases - metabolism | Phylogeny | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Adaptor Proteins, Vesicular Transport - metabolism | Recombinant Fusion Proteins - metabolism | Multiprotein Complexes - metabolism | RNA Interference | Tumor Suppressor Proteins - genetics | Apoptosis Regulatory Proteins - genetics | Phagosomes - ultrastructure | Cell Membrane - metabolism | Membrane Proteins - metabolism | Androstadienes - metabolism | Beclin-1 | rab GTP-Binding Proteins - metabolism | Amino Acid Sequence | Cell Line | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Phagosomes - metabolism | Apoptosis Regulatory Proteins - metabolism | Endocytosis - physiology | Phosphatidylinositol 3-Kinases - genetics | Multiprotein Complexes - chemistry | Sequence Alignment | Animals | Recombinant Fusion Proteins - genetics | Signal Transduction - physiology | Mice | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 05/2017, Volume 545, Issue 7652, pp. 108 - 111
Nine neurodegenerative diseases are caused by expanded polyglutamine (polyQ) tracts in different proteins, such as huntingtin in Huntington's disease and... 
PATHOGENESIS | CELLS | PROTEIN | MULTIDISCIPLINARY SCIENCES | MACHADO-JOSEPH-DISEASE | MUTANT HUNTINGTIN | ATAXIN-3 | INTRANUCLEAR INCLUSIONS | LC3 | MOUSE MODELS | AGGREGATION | Humans | Ubiquitin - metabolism | Male | Neurons - cytology | Autophagy | Brain - metabolism | Peptides - metabolism | Protein Domains | Ataxin-3 - chemistry | Female | Food Deprivation | Neurons - metabolism | Protein Stability | Ataxin-3 - metabolism | Disease Models, Animal | Binding, Competitive | Cell Line | Ataxin-3 - deficiency | Huntingtin Protein - metabolism | Mice, Inbred C57BL | Phagosomes - metabolism | Cells, Cultured | Mutant Proteins - genetics | Exons - genetics | Mutant Proteins - metabolism | Huntington Disease - metabolism | Huntingtin Protein - chemistry | Animals | Mutant Proteins - chemistry | Brain - pathology | Huntington Disease - genetics | Protein Binding | Mice | Huntingtin Protein - genetics | Mutation | Proteasome Endopeptidase Complex - metabolism | Beclin-1 - metabolism | Ataxin-3 - genetics | Physiological aspects | Autophagy (Cytology) | Neural circuitry | Observations | Huntingtons disease | Competition | Biotechnology | Huntingtin | Toxicity | Pathogenesis | Impairment | Biosynthesis | Kinases | Experiments | Degradation | Proteins | Scholarships & fellowships | Ataxin | Rodents | Spinocerebellar ataxia | Ataxia | Biocompatibility | Trinucleotide repeat diseases | Medical research | Starvation | Neurodegenerative diseases | Polyglutamine diseases | Huntington's disease | Neurological diseases | Machado-Joseph disease | Cell lines | Scientific imaging | Mass spectrometry | Phagocytosis | Index Medicus
Journal Article