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salt-induced apoptosis (60) 60
humans (55) 55
animals (43) 43
index medicus (38) 38
apoptosis (35) 35
biochemistry & molecular biology (23) 23
gastroenterology & hepatology (20) 20
apoptosis - drug effects (18) 18
male (18) 18
oxidative stress (17) 17
rats (16) 16
bile acids (15) 15
activation (14) 14
apoptosis - physiology (14) 14
acid-induced apoptosis (13) 13
salt-induced hypertension (13) 13
growth-factor receptor (11) 11
nf-kappa-b (11) 11
bile acids and salts - metabolism (10) 10
deoxycholic acid - pharmacology (10) 10
hepatocyte apoptosis (10) 10
hepatocytes - metabolism (10) 10
oncology (10) 10
phosphorylation (10) 10
rat hepatocytes (10) 10
bile-acids (9) 9
cell biology (9) 9
cytochrome-c release (9) 9
liver (9) 9
physiology (9) 9
research (9) 9
ursodeoxycholic acid (9) 9
biophysics (8) 8
colonic neoplasms - pathology (8) 8
expression (8) 8
hypertension (8) 8
mitochondria - metabolism (8) 8
pharmacology & pharmacy (8) 8
rats, wistar (8) 8
reactive oxygen species - metabolism (8) 8
signal transduction - physiology (8) 8
caspases - metabolism (7) 7
cell line, tumor (7) 7
fas receptor - metabolism (7) 7
liver - metabolism (7) 7
nadph oxidase isoforms (7) 7
reactive oxygen species (7) 7
analysis (6) 6
cell death (6) 6
cell line (6) 6
deoxycholic acid (6) 6
epidermal growth factor (6) 6
epithelial cells - metabolism (6) 6
hepatocytes - cytology (6) 6
hepatocytes - drug effects (6) 6
induced hepatocyte apoptosis (6) 6
mitochondrial permeability transition (6) 6
models, biological (6) 6
nitric-oxide (6) 6
nitric-oxide synthase (6) 6
physiological aspects (6) 6
tumor cells, cultured (6) 6
tyrosine phosphorylation (6) 6
bile acids and salts - pharmacology (5) 5
biochemistry, general (5) 5
biotechnology & applied microbiology (5) 5
cancer (5) 5
cd95 (5) 5
cells (5) 5
cells, cultured (5) 5
deoxycholic-acid (5) 5
dna-damage (5) 5
family kinase yes (5) 5
hct116 cells (5) 5
inflammation (5) 5
isolated rat hepatocytes (5) 5
liver-injury (5) 5
mice (5) 5
mitochondria (5) 5
nadph oxidases - metabolism (5) 5
necrosis (5) 5
protein-kinase-c (5) 5
rats, sprague-dawley (5) 5
receptor (5) 5
signal transduction - drug effects (5) 5
toxicology (5) 5
adenocarcinoma (4) 4
caspase inhibitors (4) 4
chemical properties (4) 4
colon - metabolism (4) 4
deoxycholate (4) 4
deoxycholate-induced apoptosis (4) 4
deoxycholic acid - toxicity (4) 4
disease models, animal (4) 4
endosomal acidification (4) 4
fas (4) 4
female (4) 4
glycochenodeoxycholic acid - pharmacology (4) 4
hepatic mitochondria (4) 4
jnk (4) 4
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1. Full Text Cathepsin-regulated apoptosis
by Chwieralski, C E and Welte, T and Bühling, F
Apoptosis, ISSN 1360-8185, 2/2006, Volume 11, Issue 2, pp. 143 - 149
Apoptosis can be mediated by different mechanisms. There is growing evidence that different proteolytic enzymes are involved in the regulation of apoptosis.... 
Biochemistry, general | protease | Medicine & Public Health | cathepsins | Cancer Research | Oncology | apoptosis | lysosome | Virology | Cell Biology | Cathepsins | Protease | Lysosome | Apoptosis | INDUCED CELL-DEATH | SALT-INDUCED APOPTOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | DEPENDENT APOPTOSIS | CELL BIOLOGY | BLEOMYCIN-INDUCED APOPTOSIS | MOUSE ALVEOLAR MACROPHAGES | CYTOCHROME-C RELEASE | CASPASE ACTIVATION | T-LYMPHOCYTES | CYSTEINE PROTEASES | MEDIATED HEPATOCYTE APOPTOSIS | Endopeptidases - metabolism | Animals | Lysosomes - metabolism | Cathepsins - classification | Cathepsins - metabolism | Models, Biological | Humans | Enzyme Activation | Proteins | Cellular biology
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2. Full Text Cell Death Independent of Caspases: A Review
by Linda E. Bröker and Frank A.E. Kruyt and Giuseppe Giaccone
Clinical Cancer Research, ISSN 1078-0432, 05/2005, Volume 11, Issue 9, pp. 3155 - 3162
Patterns of cell death have been divided into apoptosis, which is actively executed by specific proteases, the caspases, and accidental necrosis. However,... 
death pathway | programmed cell death | apoptosis | APOPTOSIS-INDUCING FACTOR | BREAST-CANCER CELLS | TUMOR-NECROSIS-FACTOR | REDUCED AUTOPHAGIC ACTIVITY | SALT-INDUCED APOPTOSIS | LYSOSOMAL MEMBRANE PERMEABILIZATION | ONCOLOGY | CATHEPSIN-B CONTRIBUTES | STRESS-INDUCED APOPTOSIS | CYTOCHROME-C RELEASE | MEDIATED HEPATOCYTE APOPTOSIS | Neoplasms - metabolism | Apoptosis - drug effects | Humans | Endoplasmic Reticulum - metabolism | Mitochondria - metabolism | Cathepsin D - metabolism | Necrosis | Neoplasms - drug therapy | Animals | Caspases - metabolism | Lysosomes - metabolism | Models, Biological | Antineoplastic Agents - pharmacology | Apoptosis - physiology | Neoplasms - pathology
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3. Full Text Bile Acid-induced Apoptosis in Hepatocytes Is Caspase-6-dependent
by Christian Rust and Nadine Wild and Carina Bernt and Timo Vennegeerts and Ralf Wimmer and Ulrich Beuers
Journal of Biological Chemistry, ISSN 0021-9258, 01/2009, Volume 284, Issue 5, pp. 2908 - 2916
Apoptosis induced by hydrophobic bile acids is thought to contribute to liver injury during cholestasis. Caspase-6 is an executioner caspase that also appears... 
RECEPTOR-MEDIATED APOPTOSIS | GROWTH-FACTOR RECEPTOR | SALT-INDUCED APOPTOSIS | ACTIVATION | CD95 | URSODEOXYCHOLIC ACID | RAT HEPATOCYTES | BIOCHEMISTRY & MOLECULAR BIOLOGY | LIVER | HEPATOMA-CELLS | FAS | Caspase 6 - metabolism | Cell Line | Apoptosis - drug effects | Humans | Gene Silencing | Rats | DNA Primers | Hepatocytes - cytology | Animals | Base Sequence | Glycochenodeoxycholic Acid - pharmacology | RNA, Small Interfering | Enzyme Activation | Hepatocytes - drug effects | Hepatocytes - enzymology
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4. Full Text Mastocarcinoma therapy synergistically promoted by lysosome dependent apoptosis specifically evoked by 5-Fu@nanogel system with passive targeting and pH activatable dual function
by Zhu, Xiandi and Sun, Yn and Chen, Huaiwen and Chen, Di and Li, Jingfeng and Li, Wei and Dong, Xia and Wang, Ying and Wang, Jie and Zhang, Fulei and Dai, Jinaxin and Pirraco, Rogério P and Guo, Shangjing and Marques, Alexandra P and Reis, Rui L
Journal of Controlled Release, ISSN 0168-3659, 05/2017, Volume 254, pp. 107 - 118
This manuscript describes a synergistic therapy for mastocarcinoma by pH and temperature dual-sensitive nanogel, and effects of microstructure, composition and... 
Passive targeting | Drug delivery | Nanogel | Mastocarcinoma therapy | Apoptosis | SALT-INDUCED APOPTOSIS | GENE DELIVERY | DRUG-DELIVERY | RELEASE | POLYMERIC MICELLES | INTRACELLULAR UPTAKE | CANCER | CHEMISTRY, MULTIDISCIPLINARY | STIMULI-RESPONSIVE NANOCARRIERS | CELL-DEATH | PHARMACOLOGY & PHARMACY | NANOGELS | Caspase 9 - metabolism | Apoptosis - drug effects | Humans | Cell Membrane Permeability | Antineoplastic Agents - administration & dosage | Molecular Targeted Therapy | Drug Carriers | Fluorouracil - administration & dosage | Lysosomes - metabolism | Imines - chemistry | Membrane Potential, Mitochondrial | Female | Polyethylenes - chemistry | Gels | Cytochromes c - metabolism | Cathepsin B - metabolism | Mitochondria - metabolism | Mitochondria - drug effects | Breast Neoplasms - drug therapy | Particle Size | Animals | Mice, Nude | Cell Line, Tumor | Nanostructures - chemistry | Mice, Inbred BALB C | Hydrogen-Ion Concentration | Cytochrome c | Enzymes | Biological products | Cathepsins | Permeability | Hydrogen-ion concentration
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5. Full Text Lysosomal membrane permeabilization in cell death
by Boya, P and Kroemer, G
Oncogene, ISSN 0950-9232, 10/2008, Volume 27, Issue 50, pp. 6434 - 6451
Mitochondrial outer membrane permeabilization ( MOMP) constitutes one of the major checkpoint(s) of apoptotic and necrotic cell death. Recently, the... 
Lysosomal membrane permeabilization | Cathepsins | Programmed cell death | Autophagy | Apoptosis | SALT-INDUCED APOPTOSIS | OXIDATIVE STRESS | autophagy | PHOTODYNAMIC THERAPY | cathepsins | BIOCHEMISTRY & MOLECULAR BIOLOGY | lysosomal membrane permeabilization | apoptosis | CATHEPSIN-DEPENDENT APOPTOSIS | CELL BIOLOGY | PROTEASE INHIBITOR 2A | BREAST-CANCER CELLS | TUMOR-NECROSIS-FACTOR | ONCOLOGY | ARYL-HYDROCARBON RECEPTOR | GENETICS & HEREDITY | TRAIL-INDUCED APOPTOSIS | programmed cell death | CYTOCHROME-C RELEASE | Animals | Intracellular Membranes - physiology | Signal Transduction | Humans | Cell Death | Cell Membrane Permeability | Neoplasms - physiopathology | Lysosomes - physiology | Physiological aspects | Research | Cell death | Membrane potentials | Risk factors | Mitochondrial membranes | Oncology | Genetics | Membranes | Cellular biology
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6. Full Text Role of the bicarbonate-responsive soluble adenylyl cyclase in cholangiocyte apoptosis in primary biliary cholangitis; a new hypothesis
by Chang, Jung-Chin and Go, Simei and Verhoeven, Arthur J and Beuers, Ulrich and Oude Elferink, Ronald P.J
BBA - Molecular Basis of Disease, ISSN 0925-4439, 04/2018, Volume 1864, Issue 4, pp. 1232 - 1239
Primary biliary cholangitis (PBC) is a chronic fibrosing cholangiopathy characterized by an autoimmune stereotype and defective biliary bicarbonate secretion... 
miR-506 | Primary biliary cholangitis | Anion exchanger 2 | Soluble adenylyl cyclase | Bile salt | Apoptosis | SALT-INDUCED APOPTOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | PULMONARY ENDOTHELIAL BARRIER | ACID-INDUCED APOPTOSIS | OVARIAN-CANCER | BIOPHYSICS | URSODEOXYCHOLIC ACID | SMOOTH-MUSCLE-CELLS | ANION-EXCHANGER 2 | CYTOCHROME-C RELEASE | GENOME-WIDE ASSOCIATION | PRIMARY SCLEROSING CHOLANGITIS | Chloride-Bicarbonate Antiporters - genetics | Up-Regulation | Epithelial Cells - metabolism | Bile Ducts - metabolism | Humans | MicroRNAs - metabolism | Autoimmune Diseases - etiology | Bile Ducts - cytology | Signal Transduction - immunology | Female | Autoimmune Diseases - pathology | Cholangitis - pathology | Genes, X-Linked - genetics | Bile Acids and Salts - metabolism | Epithelial Cells - pathology | Signal Transduction - genetics | Adenylyl Cyclases - metabolism | Cholangitis - etiology | Chloride-Bicarbonate Antiporters - metabolism | Epigenesis, Genetic - genetics | Epigenesis, Genetic - immunology | Epithelial Cells - immunology | Bicarbonates - metabolism | MicroRNAs - genetics | Bile Ducts - immunology
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7. Full Text CD95 death receptor and epidermal growth factor receptor (EGFR) in liver cell apoptosis and regeneration
by Reinehr, Roland and Häussinger, Dieter
Archives of Biochemistry and Biophysics, ISSN 0003-9861, 2012, Volume 518, Issue 1, pp. 2 - 7
► In liver, CD95 and EGFR signaling are interconnected. ► CD95 mediates apoptosis in hepatocytes but proliferation in hepatic stellate cells. ► JNK provides a... 
Fas | CD95 | JNK | Liver regeneration | EGFR | Apoptosis | NADPH OXIDASE ISOFORMS | HEPATOCYTE APOPTOSIS | SALT-INDUCED APOPTOSIS | TYROSINE PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | FAMILY KINASE YES | MEMBRANE TRAFFICKING | ENDOSOMAL ACIDIFICATION | HEPATIC STELLATE CELLS | HYPEROSMOTIC ACTIVATION | BIOPHYSICS | DEPENDENT ACTIVATION | Regeneration | Receptor, Epidermal Growth Factor - metabolism | Animals | Cell Proliferation | Liver - enzymology | Humans | Liver - metabolism | Liver - physiology | Liver - cytology | fas Receptor - metabolism | Hep G2 Cells | Cells | Epidermal growth factor
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8. Full Text Deoxycholic and chenodeoxycholic bile acids induce apoptosis via oxidative stress in human colon adenocarcinoma cells
by Barrasa, Juan Ignacio and Olmo, Nieves and Pérez-Ramos, Pablo and Santiago-Gómez, Angélica and Lecona, Emilio and Turnay, Javier and Antonia Lizarbe, M
Apoptosis, ISSN 1360-8185, 10/2011, Volume 16, Issue 10, pp. 1054 - 1067
The continuous exposure of the colonic epithelium to high concentrations of bile acids may exert cytotoxic effects and has been related to pathogenesis of... 
Biochemistry, general | Reactive oxygen species | Biomedicine | Bile acids | Colon adenocarcinoma | Oncology | Cancer Research | Caspases | Cell Biology | Virology | Apoptosis | Colon adenocarcino M.A | HEPATOCYTE APOPTOSIS | SALT-INDUCED APOPTOSIS | RAT HEPATOCYTES | PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | INVOLVEMENT | CELL BIOLOGY | CYTOCHROME-C | MITOCHONDRIAL PERMEABILITY TRANSITION | EPITHELIAL-CELLS | BUTYRATE | EXPRESSION | Adenocarcinoma - pathology | Caspase 9 - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Cell Survival | Humans | Oxidative Stress - physiology | Caspase 3 - metabolism | bcl-2-Associated X Protein - metabolism | Deoxycholic Acid - toxicity | Mitochondria - drug effects | Membrane Potential, Mitochondrial - drug effects | Chenodeoxycholic Acid - toxicity | Necrosis - chemically induced | Deoxycholic Acid - pharmacology | Colonic Neoplasms - pathology | Cell Line, Tumor | Chenodeoxycholic Acid - pharmacology | Oxidative Stress - drug effects | Oxidases | Adenocarcinoma | Oxidative stress | Colon cancer | Permeability | Deoxycholic acid | Index Medicus
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9. Full Text Protein kinase Cδ protects against bile acid apoptosis by suppressing proapoptotic JNK and BIM pathways in human and rat hepatocytes
by Webster, Cynthia R. L and Johnston, Andrea N and Sawkat Anwer, M
American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, 12/2014, Volume 307, Issue 12, pp. G1207 - G1215
Retained bile acids, which are capable of inducing cell death, activate protein kinase C delta (PKC-delta) in hepatocytes. In nonhepatic cells, both pro-and... 
Glycochenodeoxycholate | BCl2 proteins | Cell death | Exchange protein activated by cAMP | HUH7 | glycochenodeoxycholate | SURVIVAL | CELLS | SALT-INDUCED APOPTOSIS | ACTIVATION | PHYSIOLOGY | ISOFORMS | exchange protein activated by cAMP | cell death | PHOSPHORYLATION | RECEPTOR | MECHANISMS | PKC-DELTA | GROWTH | GASTROENTEROLOGY & HEPATOLOGY | Proto-Oncogene Proteins - metabolism | Apoptosis - drug effects | Humans | Rats | JNK Mitogen-Activated Protein Kinases - metabolism | Mitochondria - metabolism | Protein Transport - drug effects | Hepatocytes - metabolism | Mitochondria - drug effects | Apoptosis Regulatory Proteins - metabolism | Protein Kinase C-delta - metabolism | Animals | Bcl-2-Like Protein 11 | Signal Transduction - drug effects | Glycochenodeoxycholic Acid - pharmacology | Signal Transduction - physiology | Cell Membrane - metabolism | Membrane Proteins - metabolism | Apoptosis - physiology | Phosphorylation - drug effects | Cell Membrane - drug effects | Hepatocytes - drug effects | Liver and Biliary Tract
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10. Full Text Hydrophobic bile acid apoptosis is regulated by sphingosine-1-phosphate receptor 2 in rat hepatocytes and human hepatocellular carcinoma cells
by Webster, Cynthia R. L and Anwer, M. Sawkat
American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, 05/2016, Volume 310, Issue 10, pp. G865 - G873
Webster CR, Anwer MS. Hydrophobic bile acid apoptosis is regulated by sphingosine-1-phosphate receptor 2 in rat hepatocytes and human hepatocellular carcinoma... 
Glycochenodeoxycholate | Akt | Hepatocyte apoptosis | Sphingosine- 1-phosphate receptor | JNK | glycochenodeoxycholate | sphingosine-1-phosphate receptor | SALT-INDUCED APOPTOSIS | ACTIVATION | PHYSIOLOGY | THYROID-HORMONE | PROTECTS | GLYCOGEN-SYNTHASE | FAS RECEPTOR | INHIBITION | LIVER-INJURY | hepatocyte apoptosis | SPHINGOSINE KINASE 2 | GASTROENTEROLOGY & HEPATOLOGY | 1-PHOSPHATE | Receptors, Lysosphingolipid - antagonists & inhibitors | Rats, Wistar | Humans | Cells, Cultured | Rats | Male | Hepatocytes - metabolism | MAP Kinase Signaling System | Animals | MAP Kinase Kinase 4 - metabolism | Glycochenodeoxycholic Acid - toxicity | Liver Neoplasms - metabolism | Cell Line, Tumor | Pyridines - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Receptors, Lysosphingolipid - metabolism | Apoptosis | Carcinoma, Hepatocellular - metabolism | Glycochenodeoxycholic Acid - metabolism | Pyrazoles - pharmacology | Bile acids | Cancer cells | Physiological aspects | Physiological research | Research | Hepatoma | Pathophysiology | Liver and Biliary Tract Physiology
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11. Full Text Characterization of Enantiomeric Bile Acid-induced Apoptosis in Colon Cancer Cell Lines
by Bryson W. Katona and Shrikant Anant and Douglas F. Covey and William F. Stenson
Journal of Biological Chemistry, ISSN 0021-9258, 01/2009, Volume 284, Issue 5, pp. 3354 - 3364
Bile acids are steroid detergents that are toxic to mammalian cells at high concentrations; increased exposure to these steroids is pertinent in the... 
ELECTRON-TRANSPORT CHAIN | DEOXYCHOLIC-ACID | HEPATOCYTE APOPTOSIS | CASPASE-8 ACTIVATION | SALT-INDUCED APOPTOSIS | OXIDATIVE STRESS | LIVER-MITOCHONDRIA | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEPATIC MITOCHONDRIA | INDUCED CYTOTOXICITY | PERMEABILITY TRANSITION | Adenocarcinoma - pathology | Bile Acids and Salts - pharmacology | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Stereoisomerism | Humans | Bile Acids and Salts - chemistry | Caspase Inhibitors | Blotting, Western | Colonic Neoplasms - pathology | Cysteine Proteinase Inhibitors - pharmacology | Fluorescent Antibody Technique | Cell Line, Tumor | Index Medicus
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12. Full Text Nicotine increases oxidative stress, activates NF-κB and GRP78, induces apoptosis and sensitizes cells to genotoxic/xenobiotic stresses by a multiple stress inducer, deoxycholate: relevance to colon carcinogenesis
by Crowley-Weber, Cara L and Dvorakova, Katerina and Crowley, Cheray and Bernstein, Harris and Bernstein, Carol and Garewal, Harinder and Payne, Claire M
Chemico-Biological Interactions, ISSN 0009-2797, 2003, Volume 145, Issue 1, pp. 53 - 66
Epidemiologic studies indicate that environmental (smoking) and dietary factors (high fat) contribute to carcinogenesis in many organ systems. The aim of our... 
ER stress | Bile acids | Nicotine | Mitochondrial membrane potential | Apoptosis | nicotine | SALT-INDUCED APOPTOSIS | CANCER RISK | BIOCHEMISTRY & MOLECULAR BIOLOGY | mitochondrial membrane potential | DNA-DAMAGE | apoptosis | ACID-INDUCED APOPTOSIS | COLORECTAL MUCOSA | BILE-SALT | TUMOR PROMOTION | bile acids | ARYL-HYDROCARBON RECEPTOR | NITRIC-OXIDE | RESISTANCE | PHARMACOLOGY & PHARMACY | TOXICOLOGY
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