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The Journal of Cell Biology, ISSN 0021-9525, 12/2001, Volume 155, Issue 6, pp. 1003 - 1015
Enhanced formation of reactive oxygen species (ROS), superoxide ( O2· -), and hydrogen peroxide ( H2 O2) may result in either apoptosis or other forms of cell... 
Hep G2 cells | Depolarization | Mitochondria | Reactive oxygen species | Antibodies | Fluorescence | Liposomes | Cytosol | Cells | Apoptosis | VDAC | Superoxide anion | Cytochrome c, apoptosis | OXIDATIVE STRESS | ACTIVATION | TRANSITION PORE | PROTEIN | INDUCED APOPTOSIS | mitochondria | apoptosis | CELL BIOLOGY | PROGRAMMED CELL-DEATH | NECROSIS | INHIBITION | BAX | cytochrome c | superoxide anion | BCL-X(L) PREVENTS | Mitochondria - enzymology | Oxidants - pharmacology | Intracellular Membranes - enzymology | Humans | Porins - metabolism | Liver Neoplasms | Mitochondria - ultrastructure | Proto-Oncogene Proteins c-bcl-2 - metabolism | Tumor Cells, Cultured - enzymology | Caspases - metabolism | Transfection | Adenosine Triphosphate - metabolism | Superoxides - metabolism | Caspase 3 | Voltage-Dependent Anion Channels | Cytochrome c Group - genetics | Hydrogen Peroxide - pharmacology | Mitochondria - drug effects | Microscopy, Electron | Cytochrome c Group - metabolism | Cell Membrane Permeability - physiology | Cell Membrane Permeability - drug effects | Liposomes - metabolism | Intracellular Membranes - drug effects | Apoptosis - physiology | Carcinoma, Hepatocellular | Tumor Cells, Cultured - cytology | Cell research | Cell death | Analysis | Physiological aspects | Cytochromes | Superoxide | superoxide anion; mitochondria; VDAC; cytochrome c; apoptosis
Journal Article
Journal Article
Cell Calcium, ISSN 0143-4160, 09/2018, Volume 74, pp. 86 - 93
Journal Article
JOURNAL OF CLINICAL INVESTIGATION, ISSN 0021-9738, 02/2013, Volume 123, Issue 2, pp. 887 - 902
During sepsis, acute lung injury (ALI) results from activation of innate immune cells and endothelial cells by endotoxins, leading to systemic inflammation... 
UNITED-STATES | MEDICINE, RESEARCH & EXPERIMENTAL | CA2+ INFLUX | ACTIVATION | INOSITOL 1,4,5-TRISPHOSPHATE | PROTEIN | ENDOTHELIAL-CELLS | GENE-EXPRESSION | TNF-ALPHA | CALCIUM SENSORS STIM1 | S-GLUTATHIONYLATION | Reactive Oxygen Species - metabolism | Membrane Glycoproteins - metabolism | NADPH Oxidases - metabolism | Male | Sepsis - complications | Gene Knockdown Techniques | NADPH Oxidases - deficiency | Membrane Glycoproteins - antagonists & inhibitors | Acute Lung Injury - prevention & control | NADPH Oxidases - genetics | Female | Acute Lung Injury - metabolism | Calcium Signaling | Thiadiazoles - pharmacology | Stromal Interaction Molecule 1 | Lipopolysaccharides - toxicity | Calcium Channels | Signal Transduction | NADPH Oxidases - antagonists & inhibitors | NFATC Transcription Factors - metabolism | Cells, Cultured | Inositol 1,4,5-Trisphosphate Receptors - deficiency | Acute Lung Injury - pathology | NADPH Oxidase 2 | Membrane Glycoproteins - genetics | Mice, Knockout | Animals | Endothelium, Vascular - metabolism | Models, Biological | Anilides - pharmacology | Endothelium, Vascular - pathology | Mice | Acute Lung Injury - etiology | Inositol 1,4,5-Trisphosphate Receptors - genetics | Membrane Glycoproteins - deficiency | Blood vessels | Physiological aspects | Inflammation | Cellular signal transduction | Research | Risk factors | Lipopolysaccharides
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 07/2014, Volume 449, Issue 4, pp. 377 - 383
Journal Article