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The Journal of Cell Biology, ISSN 0021-9525, 12/2002, Volume 159, Issue 5, pp. 739 - 745
Journal Article
The EMBO Journal, ISSN 0261-4189, 08/2000, Volume 19, Issue 16, pp. 4310 - 4322
Journal Article
Cardiovascular Research, ISSN 0008-6363, 04/2011, Volume 90, Issue 1, pp. 105 - 112
Aims We have investigated Ca2+ signalling generated by aldosterone-induced T-type current (I-CaT), the effects of I-CaT in neonatal cardiomyocytes, and a... 
Protein phosphatase | Gene expression | Cav3.1 channel | Glucocorticoid receptor | Apoptosis | RAT CARDIOMYOCYTES | PATHWAYS | CARDIAC & CARDIOVASCULAR SYSTEMS | PROTEIN | INDUCED APOPTOSIS | CARDIAC MYOCYTES | HEART-FAILURE | VASCULAR SMOOTH-MUSCLE | HYPERTROPHY | CALCIUM-CHANNELS | EXPRESSION | Caspase 9 - metabolism | Rats, Wistar | Cardiomegaly - pathology | Male | Receptors, Glucocorticoid - metabolism | RNA, Messenger - metabolism | Necrosis | Myocytes, Cardiac - enzymology | Proto-Oncogene Proteins c-bcl-2 - metabolism | Aldosterone - metabolism | Flow Cytometry | Calcium Channels, T-Type - metabolism | Time Factors | Transcription, Genetic | Calcium Channels, T-Type - genetics | Calcium Signaling | Disease Models, Animal | Animals, Newborn | Cells, Cultured | Rats | Cardiomegaly - enzymology | Myocytes, Cardiac - pathology | Animals | Membrane Potentials | Cyclic AMP Response Element-Binding Protein - metabolism | Protein Phosphatase 2 - metabolism | Enzyme Activation | bcl-X Protein - metabolism | Heart | Flow cytometry | Neonates | Animal models | Bcl-2 protein | Phosphoprotein phosphatase | Calcium channels (voltage-gated) | Stenosis | Aldosterone | Cyclic AMP response element-binding protein | Calcium signalling | cardiomyocytes | Cell activation | Bcl-x protein | Feedback | Transcription activation | Caspase-9 | Heart diseases | Index Medicus | Original
Journal Article
PLoS ONE, ISSN 1932-6203, 2014, Volume 9, Issue 9, pp. e105070 - e105070
Nephrotoxicity is a dose-dependent side effect of cisplatin limiting its clinical usage in the field of cancer chemotherapy. Fisetin is a bioactive flavonoid... 
ACUTE KIDNEY INJURY | OXIDATIVE STRESS | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | MITOCHONDRIAL DYSFUNCTION | PATHOLOGICAL ROLE | MECHANISMS | MICE | RENAL INJURY | CELL-DEATH | PROTECTS | Tumor Necrosis Factor-alpha - metabolism | Phosphorylation | Caspase 9 - genetics | Caspase 9 - metabolism | Kidney - pathology | Blood Urea Nitrogen | Tumor Necrosis Factor-alpha - genetics | Caspase 3 - metabolism | Male | Cytochromes c - genetics | I-kappa B Proteins - metabolism | I-kappa B Proteins - genetics | Transcription Factor RelA - genetics | Antineoplastic Agents - toxicity | Proto-Oncogene Proteins c-bcl-2 - metabolism | Kidney - metabolism | Cisplatin - toxicity | Caspase 3 - genetics | Flavonoids - pharmacology | Cisplatin - antagonists & inhibitors | NF-KappaB Inhibitor alpha | Kidney - drug effects | Signal Transduction | Cytochromes c - metabolism | Gene Expression Regulation | Rats | Antioxidants - pharmacology | Flavonoids - pharmacokinetics | Rats, Sprague-Dawley | Animals | Nitric Oxide Synthase Type II - genetics | Transcription Factor RelA - metabolism | Creatinine - blood | Peroxidase - genetics | Antioxidants - pharmacokinetics | Proto-Oncogene Proteins c-bcl-2 - genetics | Nitric Oxide Synthase Type II - metabolism | Peroxidase - metabolism | Cytochrome | Bcl-2 protein | Syngeneic grafts | C protein | Cytotoxicity | Cytosol | Caspase-3 | NAD(P)H oxidase | Antioxidants | Proteins | Elevation | Mitochondria | Enzymatic activity | Animal tissues | Bioindicators | Medical research | NF-κB protein | Committees | Gene expression | Studies | Cytochrome c | Urea | Chemistry | Chemotherapy | Flavonoids | Caspase-9 | Biomarkers | Kidney transplantation | Oxidative stress | Enzyme activity | Bax protein | Platinum | Rodents | CYBB protein | Peroxidase | Pharmaceutical sciences | Creatinine | Translocation | Antiinflammatory agents | Kidneys | Caspase | Inflammation | Pharmacology | Cisplatin | Acids | Apoptosis | Cancer | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2014, Volume 9, Issue 7, pp. e101579 - e101579
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 07/2014, Volume 450, Issue 1, pp. 526 - 531
Journal Article
Journal of Neurochemistry, ISSN 0022-3042, 12/2010, Volume 115, Issue 6, pp. 1421 - 1433
P>Type I interferons (IFNs) are known to cause neuropsychiatric side effects, which have been proposed to be mediated by either peripheral actions or... 
JAK–STAT signaling | apoptosis | PI3K/Akt pathway | human neuroblastoma cells | PKR | type I interferons | JAK-STAT signaling | PHOSPHATIDYLINOSITOL 3-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | DEPENDENT PROTEIN-KINASE | ALPHA | Akt pathway | NEUROSCIENCES | CYTOKINE-INDUCED DEPRESSION | PI3K | GROWTH | DEPHOSPHORYLATION | PROMOTES SURVIVAL | CENTRAL-NERVOUS-SYSTEM | INHIBITOR | INSULIN-RECEPTOR SUBSTRATE-1 | STAT1 Transcription Factor - physiology | Phosphatidylinositol 3-Kinase - physiology | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Humans | Neuroblastoma - enzymology | Interferon-beta - physiology | Janus Kinases - metabolism | Proto-Oncogene Proteins c-akt - physiology | Down-Regulation - physiology | STAT1 Transcription Factor - metabolism | Animals | Janus Kinases - physiology | Cell Line, Tumor | Signal Transduction - physiology | Mice | Neuroblastoma - metabolism | Apoptosis - physiology | Neuroblastoma - pathology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus | eIF-2 kinase | Phosphorylation | Tyk2 protein | Transcription | AKT protein | Glial cells | Caspase-3 | Neuroblastoma cells | Signal transduction | Neurotoxicity | Ribose | DNA fragmentation | Janus kinase | Stat1 protein | Tyrosine | Cell survival | Cytokines | Neurons | 1-Phosphatidylinositol 3-kinase | Cytochrome c | Side effects | beta -Interferon | Protein kinase | Caspase-9 | Interferon | Apoptosis
Journal Article
by Lu, W and Zhao, Y and Kong, Y and Zhang, W and Ma, W and Li, W and Wang, K
Clinical and Experimental Dermatology, ISSN 0307-6938, 08/2018, Volume 43, Issue 6, pp. 667 - 674
BackgroundOxidative stress is one possible pathogenic event in vitiligo that induces melanocyte destruction. Geniposide exerts certain antioxidant effects on... 
VITILIGO | INVOLVEMENT | INJURY | IMPROVEMENT | RECEPTOR | PC12 CELLS | STRESS | EXPRESSION | NEUROPROTECTION | PROTECTS | DERMATOLOGY | Antioxidants | Enzymes | Superoxide | Oxidative stress | Hydrogen peroxide | Bax protein | Caspase | Melanocytes | AKT protein | Superoxide dismutase | Caspase-3 | 1-Phosphatidylinositol 3-kinase | Signal transduction | Vitiligo | Catalase | Caspase-9 | Apoptosis
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2013, Volume 8, Issue 12, pp. e83508 - e83508
Neuronal cells are susceptible to many stresses, which will cause the apoptosis and neurodegenerative diseases. The precise molecular mechanism behind the... 
APOPTOSIS | RETINOIC ACID | PHOSPHORYLATION | ALZHEIMERS-DISEASE | CASPASE-9 ACTIVATION | MULTIDISCIPLINARY SCIENCES | LIPID RAFTS | PEROXISOME BIOGENESIS DISORDERS | ADULT MICE | BINDING | DEFICIENCY | Cell Survival - drug effects | Apoptosis - drug effects | Neurons - cytology | Extracellular Signal-Regulated MAP Kinases - metabolism | Enzyme Activation - drug effects | Hippocampus - cytology | Proteolysis - drug effects | Animals | Caspases - metabolism | Signal Transduction - drug effects | Cell Line, Tumor | Mice | Neurons - metabolism | Cell Death - drug effects | Phosphorylation - drug effects | Neurons - drug effects | Plasmalogens - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Tretinoin - pharmacology | Nervous system diseases | Biochemistry | Neurons | Protein kinases | Apoptosis | Brain | Phosphorylation | Caspase-12 | AKT protein | Activation | Neuroblastoma | Kinases | Caspase-3 | Signal transduction | Cell activation | Cell cycle | Physiology | Inhibition | Deoxyribonucleic acid--DNA | Enzymes | Deprivation | Starvation | Cell survival | Threonine | Neurodegenerative diseases | Ethanol | Mortality | Extracellular signal-regulated kinase | Caspase | MAP kinase | Survival | 1-Phosphatidylinositol 3-kinase | Neurological diseases | Caspase-8 | Signaling | Brain research | Inhibitors | Protein kinase | Cell death | Caspase-9 | Alzheimers disease | Hippocampus | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 02/2017, Volume 114, Issue 7, pp. 1542 - 1547
Mammalian intrinsic apoptosis requires activation of the initiator caspase-9, which then cleaves and activates the effector caspases to execute cell killing.... 
Apoptosome | Caspase activation | Holoenzyme | Cryo-EM | Caspase-9 | COMPLEX | caspase-9 | MULTIDISCIPLINARY SCIENCES | RESOLUTION | APAF-1 | MODEL | CYTOCHROME-C | PROCASPASE-9 | INHIBITION | PARTICLE ELECTRON CRYOMICROSCOPY | caspase activation | MEDIATED ACTIVATION | apoptosome | cryo-EM | holoenzyme |