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Nature Cell Biology, ISSN 1465-7392, 05/2007, Volume 9, Issue 5, pp. 550 - 555
Journal Article
Nature Cell Biology, ISSN 1465-7392, 10/2015, Volume 17, Issue 10, pp. 1270 - 1281
Multidomain pro-apoptotic BAX and BAK, once activated, permeabilize mitochondria to trigger apoptosis, whereas anti-apoptotic BCL-2 members preserve... 
CYTOCHROME-C | MITOCHONDRIAL APOPTOSIS | ACTIVATION | CONFORMATIONAL-CHANGE | MEMBERS | PROAPOPTOTIC BAX | BH3 DOMAINS | PUMA | BH3-ONLY PROTEINS | MEMBRANE PERMEABILIZATION | CELL BIOLOGY | bcl-2 Homologous Antagonist-Killer Protein - genetics | Immunoblotting | BH3 Interacting Domain Death Agonist Protein - genetics | Cytochromes c - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Embryo, Mammalian - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Bcl-2-Like Protein 11 | Mitochondria - genetics | RNA Interference | Tumor Suppressor Proteins - genetics | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | bcl-2-Associated X Protein - genetics | Fibroblasts - metabolism | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cytochromes c - metabolism | Mice, Inbred C57BL | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Intestine, Small - cytology | Embryo, Mammalian - cytology | Models, Biological | Fibroblasts - cytology | Intestine, Small - metabolism | Proto-Oncogene Proteins c-bcl-2 - genetics | Apoptosis | Genotype | Genetic aspects | Properties | Cell death | Cellular control mechanisms | Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 03/2006, Volume 281, Issue 11, pp. 7260 - 7270
Journal Article
Biomaterials, ISSN 0142-9612, 2011, Volume 32, Issue 23, pp. 5438 - 5458
Abstract Oxidative stress is a major component of harmful cascades activated in neurodegenerative disorders. We sought to elucidate possible effects of... 
Advanced Basic Science | Dentistry | Oxidative stress | Mitochondria | Caspase-dependent apoptosis | Endoplasmic reticulum | Alginate oligosaccharide | PC12 cells | SIGNALING PATHWAYS | ACTIVATION | MATERIALS SCIENCE, BIOMATERIALS | ENGINEERING, BIOMEDICAL | CASCADES | P53 | DISEASES | BAX | CYTOCHROME-C RELEASE | PROTEINS | BINDING | MEMBRANE PERMEABILIZATION | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Calcium - metabolism | Glutathione - metabolism | Amyloid beta-Peptides - pharmacology | Oxidative Stress - physiology | Caspase 3 - metabolism | Endoplasmic Reticulum - metabolism | NF-kappa B - metabolism | Neurons - cytology | Peptide Fragments - pharmacology | Extracellular Signal-Regulated MAP Kinases - metabolism | PC12 Cells | Oligosaccharides - pharmacology | Proto-Oncogene Proteins c-bcl-2 - metabolism | Apoptosis Inducing Factor - pharmacology | Cell Nucleus - metabolism | Endoplasmic Reticulum - drug effects | Oxidation-Reduction - drug effects | Neurons - metabolism | Phosphorylation - drug effects | Glucuronic Acid - chemistry | Neurons - drug effects | Polysaccharide-Lyases - chemistry | Apoptosis Inducing Factor - metabolism | Cell Survival - drug effects | Cytochromes c - metabolism | Hydrogen Peroxide - pharmacology | Tumor Suppressor Protein p53 - metabolism | bcl-2-Associated X Protein - metabolism | Rats | Mitochondria - metabolism | Caspase 12 - metabolism | Hexuronic Acids - chemistry | Mitochondria - drug effects | HSP70 Heat-Shock Proteins - metabolism | Cell Shape - drug effects | Poly(ADP-ribose) Polymerases - metabolism | Animals | Models, Biological | Alginates - chemistry | NF-E2-Related Factor 2 - metabolism | HSP90 Heat-Shock Proteins - metabolism | Apoptosis - physiology | Oxidative Stress - drug effects | Cell Nucleus - drug effects | Neurosciences | Nervous system diseases | Biological products | Hydrogen peroxide | Heat shock proteins | Nerve growth factor | Superoxide | Mitochondrial DNA | Biochemistry | Antioxidants | Tumor proteins | Protein kinases | Alzheimer's disease | Apoptosis | Stresses | Surgical implants | Biomedical materials | Cell death | Cascades | Blocking | Activation | Kinases | Index Medicus
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2012, Volume 7, Issue 11, pp. e49701 - e49701
Paeoniflorin (PF), the principal component of Paeoniae Radix prescribed in traditional Chinese medicine, has been reported to exhibit many pharmacological... 
STROKE | ACTIVATION | PATHWAY | NEUROVASCULAR UNIT | MULTIDISCIPLINARY SCIENCES | FOCAL CEREBRAL-ISCHEMIA | INTRACEREBRAL HEMORRHAGE | NITRIC-OXIDE | MECHANISMS | EXPRESSION | NEUROPROTECTION | Microglia - metabolism | Tumor Necrosis Factor-alpha - blood | Tumor Necrosis Factor-alpha - genetics | Male | NF-kappa B - metabolism | Interleukin-1beta - genetics | Brain - metabolism | Inflammation - metabolism | Bridged-Ring Compounds - pharmacology | Monoterpenes | Neurons - metabolism | Disease Models, Animal | NF-kappa B - antagonists & inhibitors | bcl-2-Associated X Protein - metabolism | Rats | Brain - drug effects | Signal Transduction - drug effects | Brain Ischemia - drug therapy | Benzoates - pharmacology | Brain - pathology | Bridged-Ring Compounds - administration & dosage | Astrocytes - metabolism | Nitric Oxide Synthase Type II - metabolism | Cerebral Infarction - drug therapy | Brain Ischemia - metabolism | Cytochromes c - genetics | Hippocampus - drug effects | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | Interleukin-1beta - blood | Proto-Oncogene Proteins c-bcl-2 - metabolism | Lipoxygenase - metabolism | Cerebral Infarction - metabolism | Inflammation - drug therapy | Neurons - drug effects | bcl-2-Associated X Protein - genetics | Cerebral Infarction - pathology | Astrocytes - drug effects | Glucosides - pharmacology | Microglia - drug effects | Cytochromes c - metabolism | Benzoates - administration & dosage | Gene Expression Regulation - drug effects | Animals | Glucosides - administration & dosage | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Anti-Inflammatory Agents, Non-Steroidal - administration & dosage | Cyclooxygenase 2 - metabolism | Proto-Oncogene Proteins c-bcl-2 - genetics | Mitogen-Activated Protein Kinases - metabolism | Occlusion | Neuroprotection | Brain | Inflammatory response | Activation | Kinases | Carotid arteries | Signal transduction | Chinese medicine | Ischemia | Neurodegeneration | Cerebral blood flow | Rodents | Tumor necrosis factor-TNF | Inhibition | NF-κB protein | Stroke | Cytokines | Astrocytes | Traditional Chinese medicine | Extracellular signal-regulated kinase | MAP kinase | JNK protein | Pharmacology | Inflammation | Tumor necrosis factor-α | IL-1β | Nitric-oxide synthase | Microglia | Signaling | Brain research | Liquid oxygen | Hypoxia | Brain damage | Cyclooxygenase-2 | Laboratory animals | Apoptosis | Veins & arteries | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2013, Volume 8, Issue 2, pp. e54374 - e54374
Cadmium (Cd), one of well-known highly toxic environmental and industrial pollutants, causes a number of adverse health effects and diseases in humans. The... 
HUMAN-DISEASE | GLUCOSE | MULTIDISCIPLINARY SCIENCES | BIOLOGICAL SAMPLES | INSULIN-SECRETION | URINARY CADMIUM | RATS | DEATH | PHYSIOLOGICAL FUNCTIONS | TOXIC METALS | EXPRESSION | MAP Kinase Signaling System - physiology | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Extracellular Signal-Regulated MAP Kinases - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Insulin-Secreting Cells - metabolism | Caspases - metabolism | Insulin-Secreting Cells - cytology | p38 Mitogen-Activated Protein Kinases - metabolism | Insulin Secretion | Malondialdehyde - metabolism | Cell Line | Cell Survival - drug effects | Cytochromes c - metabolism | Cadmium - pharmacology | Rats | Mitochondria - metabolism | Mitochondria - drug effects | Mice, Inbred ICR | Insulin - metabolism | Poly(ADP-ribose) Polymerases - metabolism | Animals | Tumor Suppressor Protein p53 | Insulin-Secreting Cells - drug effects | Oxidative Stress - drug effects | Cytochrome | Transcription factors | Disease | Bcl-2 protein | p53 Protein | Acetylcysteine | Glucose | ADP | Epidemiology | Antioxidants | Toxicology | Mitochondria | Physiology | Membrane potential | Cadmium | MAP kinase | Exposure | Mammals | Insulin | Malondialdehyde | Cytochrome c | Hospitals | Cell injury | Inhibitors | Ribonucleic acids | Viability | Oxidative stress | Arsenic | Otolaryngology | Activation | Kinases | Ribose | Rodents | Cascades | Cell cycle | Pretreatment | Pollutants | Pancreas | Diabetes mellitus | Health risks | Extracellular signal-regulated kinase | c-Jun protein | Poly(ADP-ribose) polymerase | Caspase | Industrial pollution | Medicine | Polymerase | Protein kinase | Cell death | Annexin V | Intracellular | Diabetes | Apoptosis | Index Medicus
Journal Article
Journal of Molecular Biology, ISSN 0022-2836, 10/2008, Volume 382, Issue 3, pp. 790 - 801
Journal Article
Science, ISSN 0036-8075, 12/2010, Volume 330, Issue 6009, pp. 1390 - 1393
Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled. We provide in... 
T lymphocytes | Mitochondria | Cytokines | Thymocytes | Neurons | Cell death | REPORTS | Cytochromes | Mice | Potassium | Apoptosis | NEURONAL APOPTOSIS | CYTOCHROME-C | MITOCHONDRIAL APOPTOSIS | MECHANISM | MULTIDISCIPLINARY SCIENCES | BH3 DOMAINS | RELEASE | JNK PATHWAY | PROTEINS | BCL-2 FAMILY-MEMBERS | MEMBRANE PERMEABILIZATION | BH3 Interacting Domain Death Agonist Protein - deficiency | T-Lymphocytes - physiology | bcl-2-Associated X Protein - chemistry | Protein Multimerization | Stress, Physiological | bcl-2 Homologous Antagonist-Killer Protein - genetics | BH3 Interacting Domain Death Agonist Protein - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Membrane Proteins - deficiency | Caspases - metabolism | Bcl-2-Like Protein 11 | Apoptosis Regulatory Proteins - deficiency | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | Neurons - physiology | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | bcl-2-Associated X Protein - genetics | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cytochromes c - metabolism | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Permeability | Proto-Oncogene Proteins - deficiency | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Models, Biological | Cerebellum - cytology | Intracellular Membranes - metabolism | bcl-2 Homologous Antagonist-Killer Protein - chemistry | Protein research | Genetic aspects | Mitochondrial DNA | Biochemical genetics | Research | Properties | Methods | Index Medicus
Journal Article