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BBA - Molecular Basis of Disease, ISSN 0925-4439, 06/2013, Volume 1832, Issue 6, pp. 848 - 863
Sepsis is characterized by systematic inflammation and contributes to cardiac dysfunction. This study was designed to examine the effect of protein kinase B... 
Heart | ER stress | Sepsis | Akt | Contractile function | Apoptosis | OXIDATIVE STRESS | CONTRACTILE DYSFUNCTION | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | ENDOPLASMIC-RETICULUM STRESS | AUTOPHAGY | GROWTH-FACTOR I | SIGNAL-TRANSDUCTION | SYNTHASE | BIOPHYSICS | INFLAMMATORY RESPONSE | NF-KAPPA-B | Caspase 9 - genetics | Apoptosis - drug effects | Calcium - metabolism | Heat-Shock Proteins - biosynthesis | Myocardial Contraction - drug effects | bcl-2-Associated X Protein - biosynthesis | Apoptosis - genetics | Glycogen Synthase Kinase 3 beta | Heat-Shock Proteins - genetics | Phosphorylation - genetics | Caspase 3 - genetics | Phosphorylation - drug effects | Transcription Factor CHOP - biosynthesis | Proto-Oncogene Proteins c-akt - metabolism | Apoptosis Regulatory Proteins - biosynthesis | Lipopolysaccharides - toxicity | Endoplasmic Reticulum Stress - drug effects | Mice, Transgenic | Glycogen Synthase Kinase 3 - genetics | Eukaryotic Initiation Factor-2 - genetics | Mice | Enzyme Activation - genetics | Transcription Factor CHOP - genetics | Eukaryotic Initiation Factor-2 - biosynthesis | Microtubule-Associated Proteins - genetics | bcl-X Protein - genetics | Extracellular Signal-Regulated MAP Kinases - metabolism | Endoplasmic Reticulum Stress - genetics | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | Myocardial Contraction - genetics | MAP Kinase Signaling System - genetics | Apoptosis Regulatory Proteins - genetics | Caspase 3 - biosynthesis | bcl-X Protein - biosynthesis | bcl-2-Associated X Protein - genetics | Beclin-1 | Gene Expression Regulation - genetics | Myocardium - pathology | Transcription Factors - biosynthesis | Transcription Factors - genetics | Enzyme Activation - drug effects | Glycogen Synthase Kinase 3 - metabolism | Microtubule-Associated Proteins - biosynthesis | Gene Expression Regulation - drug effects | Autophagy-Related Protein 7 | Myocardium - enzymology | Animals | MAP Kinase Signaling System - drug effects | Caspase 9 - biosynthesis
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 02/2014, Volume 289, Issue 6, pp. 3126 - 3137
Background: The chemokine receptor CXCR3-B initiates inhibitory signals. Results: CXCR3-B-mediated signal induced apoptosis and inhibited autophagy of breast... 
Signal Transduction | SPLICE VARIANT | BIOCHEMISTRY & MOLECULAR BIOLOGY | I-TAC | Heme Oxygenase | HEME OXYGENASE-1 GENE | CXC CHEMOKINES | HUMAN BREAST-CANCER | Signaling | MURINE MODEL | EPITHELIAL-CELLS | Nrf2 | Nuclear Transport | TRANSCRIPTION FACTOR | EXPRESSION | Chemokines | Apoptosis | Basic-Leucine Zipper Transcription Factors - metabolism | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Humans | bcl-X Protein - genetics | Apoptosis - genetics | Breast Neoplasms - metabolism | MAP Kinase Signaling System | Heme Oxygenase-1 - genetics | Fanconi Anemia Complementation Group Proteins - metabolism | Cell Nucleus - metabolism | Protein Isoforms - metabolism | Cell Nucleus - pathology | Mitogen-Activated Protein Kinase 1 - genetics | Apoptosis Regulatory Proteins - genetics | Female | NF-E2-Related Factor 2 - genetics | Membrane Proteins - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Active Transport, Cell Nucleus - genetics | Beclin-1 | Receptors, CXCR3 - metabolism | Heme Oxygenase-1 - biosynthesis | Mitogen-Activated Protein Kinase 3 - genetics | Membrane Proteins - genetics | Alternative Splicing - genetics | Fanconi Anemia Complementation Group Proteins - genetics | p38 Mitogen-Activated Protein Kinases - genetics | Basic-Leucine Zipper Transcription Factors - genetics | Apoptosis Regulatory Proteins - metabolism | Breast Neoplasms - genetics | Cell Nucleus - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Breast Neoplasms - pathology | NF-E2-Related Factor 2 - metabolism | Receptors, CXCR3 - genetics | Cell Line, Tumor | bcl-X Protein - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Protein Isoforms - genetics
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2017, Volume 12, Issue 4, p. 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
Journal Article
Journal of Leukocyte Biology, ISSN 0741-5400, 02/2015, Volume 97, Issue 2, pp. 425 - 433
ER stress induced autophagy and decreased GRP78 expression of T lymphocytes are involved in the pathogenesis of SLE and potentially important therapeutic... 
T cells | apoptosis | SLE | PATHWAYS | SURVIVAL | ENDOPLASMIC-RETICULUM STRESS | MACROAUTOPHAGY | IMMUNOLOGY | CELL-DEATH | CELL BIOLOGY | UNFOLDED PROTEIN RESPONSE | DISEASE | HEMATOLOGY | PROMOTES | EXPRESSION | RNA, Small Interfering - genetics | Transcription Factor CHOP - genetics | Endoribonucleases - genetics | Activating Transcription Factor 6 - immunology | Humans | bcl-X Protein - genetics | eIF-2 Kinase - immunology | Male | Endoplasmic Reticulum Stress - genetics | Activating Transcription Factor 6 - genetics | Endoplasmic Reticulum Stress - immunology | Autophagy - immunology | Heat-Shock Proteins - genetics | RNA, Small Interfering - immunology | Lupus Erythematosus, Systemic - immunology | Transcription Factor CHOP - immunology | bcl-X Protein - immunology | Apoptosis Regulatory Proteins - genetics | Female | Autophagy - genetics | T-Lymphocytes - pathology | bcl-2-Associated X Protein - genetics | eIF-2 Kinase - genetics | Beclin-1 | Apoptosis Regulatory Proteins - immunology | Gene Expression Regulation - genetics | Gene Expression Regulation - immunology | Membrane Proteins - genetics | Protein-Serine-Threonine Kinases - genetics | Membrane Proteins - immunology | Heat-Shock Proteins - immunology | bcl-2-Associated X Protein - immunology | Caspase 6 - genetics | Eukaryotic Initiation Factor-2 - genetics | Lupus Erythematosus, Systemic - genetics | Protein-Serine-Threonine Kinases - immunology | T-Lymphocytes - immunology | Caspase 6 - immunology | Eukaryotic Initiation Factor-2 - immunology | Lupus Erythematosus, Systemic - pathology | Endoribonucleases - immunology
Journal Article
Journal of Molecular Medicine, ISSN 0946-2716, 6/2016, Volume 94, Issue 6, pp. 711 - 724
Recent studies have indicated a protective role of physiological autophagy in ischemic heart disease. However, the underlying mechanisms of autophagy... 
Human Genetics | miR-30a | Biomedicine | Internal Medicine | Hypoxia | Cardiomyocytes | Molecular Medicine | Exosomes | Autophagy | CIRCULATING MICRORNAS | MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | MECHANISM | MICROVESICLES | EXTRACELLULAR VESICLES | BECLIN-1 | INTERCELLULAR COMMUNICATION | GROWTH | GENETICS & HEREDITY | EXCHANGE | Exosomes - metabolism | Myocardial Infarction - genetics | MicroRNAs - antagonists & inhibitors | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Humans | Middle Aged | Male | MicroRNAs - metabolism | Hypoxia - metabolism | Cell Hypoxia | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Myocardial Infarction - pathology | Adult | Female | Autophagy - genetics | Oligoribonucleotides, Antisense - metabolism | Cell Line | Autophagy-Related Protein 12 - genetics | Paracrine Communication | Signal Transduction | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Gene Expression Regulation | Myocardial Infarction - metabolism | Autophagy-Related Protein 12 - metabolism | Myocytes, Cardiac - pathology | Hypoxia - genetics | Hypoxia - pathology | Oligoribonucleotides, Antisense - genetics | Beclin-1 - genetics | Myocytes, Cardiac - metabolism | Aged | MicroRNAs - genetics | Beclin-1 - metabolism | Autophagy (Cytology) | Heart cells | Physiological aspects | Development and progression | Genetic aspects | Research | Heart diseases
Journal Article
Molecular Cell, ISSN 1097-2765, 2011, Volume 42, Issue 1, pp. 23 - 35
Journal Article
Chemico-Biological Interactions, ISSN 0009-2797, 02/2014, Volume 208, Issue 1, pp. 47 - 57
HIMOXOL (methyl 3-hydroxyimino-11-oxoolean-12-en-28-oate) is a synthetic derivative of oleanolic acid (OA). HIMOXOL revealed the highest cytotoxic effect among... 
Breast cancer | Autophagy | HIMOXOL | Apoptosis | SIGNALING PATHWAYS | ACTIVATED PROTEIN-KINASE | TRITERPENOIDS | MECHANISM | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOWN-REGULATION | SUPPRESSES MIGRATION | DEATH | PROSTATE-CANCER | PHARMACOLOGY & PHARMACY | TOXICOLOGY | MULTIDRUG-RESISTANCE | NF-KAPPA-B | Cell Cycle - genetics | Microtubule-Associated Proteins - genetics | Apoptosis - drug effects | Microtubule-Associated Proteins - metabolism | Humans | Oleanolic Acid - analogs & derivatives | Caspase 3 - metabolism | Caspase 8 - metabolism | Cell Survival - genetics | Oleanolic Acid - pharmacology | Apoptosis - genetics | NF-kappa B - metabolism | Autophagy - drug effects | Breast Neoplasms - metabolism | Caspase 8 - genetics | Proto-Oncogene Proteins c-bcl-2 - metabolism | Cell Death - genetics | Caspase 3 - genetics | Apoptosis Regulatory Proteins - genetics | Female | Antineoplastic Agents - pharmacology | Membrane Proteins - metabolism | Autophagy - genetics | Cell Death - drug effects | bcl-2-Associated X Protein - genetics | Beclin-1 | Cell Survival - drug effects | Membrane Proteins - genetics | bcl-2-Associated X Protein - metabolism | Up-Regulation - genetics | Signal Transduction - genetics | Breast Neoplasms - drug therapy | Apoptosis Regulatory Proteins - metabolism | Up-Regulation - drug effects | Poly(ADP-ribose) Polymerases - metabolism | Breast Neoplasms - genetics | Poly(ADP-ribose) Polymerases - genetics | NF-kappa B - genetics | Signal Transduction - drug effects | Cell Line, Tumor | Mitogen-Activated Protein Kinases - genetics | Poly (ADP-Ribose) Polymerase-1 | Cell Cycle - drug effects | Proto-Oncogene Proteins c-bcl-2 - genetics | Mitogen-Activated Protein Kinases - metabolism | Tumor proteins | Cancer cells
Journal Article
Brain, ISSN 0006-8950, 2013, Volume 136, Issue 7, pp. 2173 - 2188
Machado-Joseph disease or spinocerebellar ataxia type 3, the most common dominantly-inherited spinocerebellar ataxia, results from translation of the... 
ataxin-3 | autophagy | beclin-1, Machado-Joseph disease, spinocerebellar ataxia type 3 | AUTOPHAGY GENE | PROTEIN | spinocerebellar ataxia type 3 | PHOSPHATIDYLINOSITOL 3-KINASE | SPINOCEREBELLAR ATAXIA TYPE-3 | MUTANT HUNTINGTIN | NEURODEGENERATION | NEUROSCIENCES | beclin-1 | CLINICAL NEUROLOGY | Machado-Joseph disease | ACID RAT MODEL | ACCUMULATION | HUNTINGTONS-DISEASE | TRANSGENIC MICE | Age Factors | Ataxin-3 | Machado-Joseph Disease - metabolism | Humans | Peptides - genetics | Motor Activity - drug effects | Sensation Disorders - etiology | Male | Green Fluorescent Proteins - genetics | Membrane Proteins - therapeutic use | Psychomotor Performance - physiology | Machado-Joseph Disease - complications | Transfection | Nerve Degeneration - prevention & control | Apoptosis Regulatory Proteins - genetics | Female | Membrane Proteins - metabolism | Autophagy - genetics | Nuclear Proteins - genetics | Repressor Proteins - metabolism | Disease Models, Animal | Animals, Newborn | Beclin-1 | Gene Expression Regulation - genetics | Membrane Proteins - genetics | Mice, Inbred C57BL | Cells, Cultured | Repressor Proteins - genetics | Sensation Disorders - metabolism | Mice, Transgenic | Nuclear Proteins - metabolism | Postural Balance - genetics | Dopamine and cAMP-Regulated Phosphoprotein 32 - metabolism | Nerve Tissue Proteins - genetics | Apoptosis Regulatory Proteins - metabolism | Machado-Joseph Disease - drug therapy | Nerve Tissue Proteins - metabolism | Motor Activity - genetics | Animals | Analysis of Variance | Cerebellum - cytology | Mice | Sensation Disorders - genetics | Apoptosis Regulatory Proteins - therapeutic use | Nerve Degeneration - etiology | Machado-Joseph Disease - genetics | Animal models
Journal Article
Aging Cell, ISSN 1474-9718, 10/2017, Volume 16, Issue 5, pp. 976 - 987
Summary Aging is accompanied with unfavorable geometric and functional changes in the heart involving dysregulation of Akt and autophagy. This study examined... 
cardiac geometry | contractile function | autophagy | aging | Akt | RAPAMYCIN | PROTEIN-KINASE | DIASTOLIC DYSFUNCTION | CELL BIOLOGY | GERIATRICS & GERONTOLOGY | HYPERTROPHY | LONGEVITY | OVEREXPRESSION | INSULIN-RESISTANCE | CALORIC RESTRICTION | SENESCENCE | MITOCHONDRIAL INJURY | Adaptation, Physiological | Protein Kinases - metabolism | Sirtuin 1 - metabolism | Phosphorylation | Protein Kinases - genetics | Microtubule-Associated Proteins - genetics | Calcium - metabolism | Microtubule-Associated Proteins - metabolism | Autophagy-Related Protein 7 - metabolism | Proto-Oncogene Proteins c-akt - deficiency | Atrial Remodeling - drug effects | Myocardial Contraction - drug effects | Cardiomegaly - pathology | Male | Mitochondrial Proteins - genetics | Sirtuin 1 - genetics | Autophagy - drug effects | Heterocyclic Compounds, 4 or More Rings - pharmacology | Proto-Oncogene Proteins c-akt - genetics | Mitochondrial Proteins - metabolism | Myocardium - metabolism | Membrane Proteins - metabolism | Autophagy - genetics | Forkhead Box Protein O1 - metabolism | Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism | Signal Transduction | Membrane Proteins - genetics | Gene Expression Regulation | Myocardium - pathology | Mitochondria - metabolism | Longevity - genetics | Mitochondria - pathology | Autophagy-Related Protein 7 - genetics | Sirolimus - pharmacology | Mice, Knockout | Animals | Cardiomegaly - prevention & control | Beclin-1 - genetics | Mice | Beclin-1 - metabolism | Cardiomegaly - genetics | Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics | Forkhead Box Protein O1 - genetics | Cardiomegaly - metabolism | Heart | Laws, regulations and rules | Ablation (Surgery) | AKT protein | Autophagy | Ca2+-transporting ATPase | Mitochondria | FOXO1 protein | Aging | Oxidation | Fura-2 | Acetylation | Heart diseases | Calcium (intracellular) | Echocardiography | Contractility | AKT2 protein | Cardiomyocytes | Rapamycin | Insulin | Muscle contraction | BNIP3 protein | Life span | PTEN-induced putative kinase | Parkin protein | Intracellular | PTEN protein | Phagocytosis | Hypertrophy | Original
Journal Article
Spine, ISSN 0362-2436, 2015, Volume 40, Issue 11, pp. 773 - 782
Study Design. Autophagy-related gene expression and ultrastructural features of autophagy were studied in human discs. Objective. To obtain... 
TNF-α | Disc degeneration | Intervertebral disc | PIM-2 oncogene | p62/SQSTM1 | Proinflammatory cytokines | IL-1β | Autophagy | WIPI49 | NUCLEUS PULPOSUS | intervertebral disc | proinflammatory cytokines | autophagy | TNF-alpha | TISSUE | IL-1 beta | 3-DIMENSIONAL CULTURE | MEDIATED APOPTOSIS | PROTEOGLYCAN | CLINICAL NEUROLOGY | PATHOGENESIS | OXYGEN | BIOENERGETICS | GENE-EXPRESSION | disc degeneration | SENESCENCE | ORTHOPEDICS | Protein-Serine-Threonine Kinases - analysis | RNA-Binding Proteins - genetics | Autophagy-Related Proteins | Interleukin-1beta - pharmacology | Gene Expression - drug effects | Microtubule-Associated Proteins - genetics | Cathepsin B - genetics | Humans | Middle Aged | Apoptosis Regulatory Proteins - analysis | RNA, Messenger - analysis | Infant | Male | Autophagy - drug effects | Membrane Proteins - analysis | Intervertebral Disc Degeneration - metabolism | Cysteine Endopeptidases - analysis | Intervertebral Disc Degeneration - pathology | Young Adult | Sacrum | Ubiquitin-Conjugating Enzymes - analysis | Apoptosis Regulatory Proteins - genetics | Adult | Female | Autophagy - genetics | Ubiquitin-Activating Enzymes - analysis | RNA-Binding Proteins - analysis | Intervertebral Disc Degeneration - genetics | Beclin-1 | Intervertebral Disc - ultrastructure | Ubiquitin-Activating Enzymes - genetics | Microtubule-Associated Proteins - analysis | Membrane Proteins - genetics | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Intervertebral Disc - chemistry | Presenilin-1 - genetics | Proto-Oncogene Proteins - genetics | Ubiquitin-Conjugating Enzymes - genetics | Up-Regulation - drug effects | Carrier Proteins - genetics | Tumor Necrosis Factor-alpha - pharmacology | Autophagy-Related Protein 7 | Cysteine Endopeptidases - genetics | Aged | Lumbar Vertebrae
Journal Article
Journals of Gerontology - Series A Biological Sciences and Medical Sciences, ISSN 1079-5006, 2014, Volume 69, Issue 8, pp. 1040 - 1048
Reduced lean mass and physical function is a characteristic of frailty. However, it is currently unknown if proteolysis through the E3 ubiquitin ligases and... 
Atrophy | Aging | Mobility | Mitochondrial dysfunction | Autophagy | ELDERLY INDIVIDUALS | ADULTS | SARCOPENIA | GERIATRICS & GERONTOLOGY | RESISTANCE EXERCISE | MASS | GERONTOLOGY | PROTEIN BREAKDOWN | BED REST | EXPRESSION | Phosphorylation - physiology | Sarcopenia - genetics | Microtubule-Associated Proteins - genetics | SKP Cullin F-Box Protein Ligases - genetics | Humans | Endosomal Sorting Complexes Required for Transport - genetics | Mitochondrial Proteins - genetics | Ubiquitin-Protein Ligases - physiology | Tripartite Motif Proteins | Muscular Atrophy - physiopathology | Proteolysis | Gene Expression - physiology | Genes, Tumor Suppressor - physiology | Aged, 80 and over | Apoptosis Regulatory Proteins - genetics | Female | Nedd4 Ubiquitin Protein Ligases | Beclin-1 | Cross-Sectional Studies | Membrane Proteins - genetics | Proto-Oncogene Proteins - genetics | Frail Elderly | Muscle, Skeletal - physiology | Forkhead Transcription Factors - genetics | Mitochondrial Degradation - physiology | Down-Regulation - physiology | Muscle Proteins - genetics | Sarcopenia - physiopathology | GTP Phosphohydrolases - genetics | Aged | Muscle, Skeletal - pathology | Forkhead Box Protein O3 | Ubiquitin-Protein Ligases - genetics | AMP-Activated Protein Kinases - genetics | Ubiquitin | Physiological aspects | Muscles | Aged women | Ligases
Journal Article