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PloS one, ISSN 1932-6203, 2012, Volume 7, Issue 6, p. e39586
Endoplasmic reticulum (ER) stress-induced apoptosis has been implicated in various neurodegenerative diseases including Parkinson Disease, Alzheimer Disease... 
MITOCHONDRIAL APOPTOSIS | TRANSCRIPTION FACTOR CHOP | UNFOLDED PROTEIN RESPONSE | INDUCED APOPTOSIS | KINASE | BIOLOGY | GENE-EXPRESSION | SYMPATHETIC NEURONS | DEATH | ENDOPLASMIC-RETICULUM STRESS | BH3-ONLY PROTEINS | Transcription Factor CHOP - genetics | Apoptosis - drug effects | Neurons - cytology | Bcl-2-Like Protein 11 | Forkhead Transcription Factors - metabolism | Telencephalon - drug effects | Tumor Suppressor Proteins - genetics | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | Neurons - metabolism | Neurons - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Cell Survival - physiology | Proto-Oncogene Proteins - metabolism | Cell Survival - drug effects | Tumor Suppressor Proteins - metabolism | Telencephalon - metabolism | Telencephalon - cytology | Membrane Proteins - genetics | Proto-Oncogene Proteins - genetics | Forkhead Transcription Factors - genetics | Apoptosis Regulatory Proteins - metabolism | Animals | Signal Transduction - drug effects | Tunicamycin - pharmacology | Signal Transduction - physiology | Mice | Apoptosis - physiology | Forkhead Box Protein O3 | Transcription Factor CHOP - metabolism | Endoplasmic Reticulum Stress - physiology | Nervous system diseases | Parkinson's disease | Huntington's chorea | Neurons | Tumor proteins | Protein kinases | Apoptosis | Phosphorylation | Transcription factors | Transcription | p53 Protein | Tunicamycin | Homology | AKT protein | CCAAT/enhancer-binding protein | Kinases | Proteins | Signal transduction | Mitochondria | Cell activation | Cell growth | Cascades | Rodents | Forkhead protein | Alzheimer's disease | Movement disorders | Deoxyribonucleic acid--DNA | FOXO3 protein | Stresses | Neurodegenerative diseases | Mortality | Gene expression | Stress | Neurological diseases | Pathology | Signaling | Cell death | Endoplasmic reticulum | CHOP protein | BIM protein | Deoxyribonucleic acid | DNA
Journal Article
Journal Article
Cancer letters, ISSN 0304-3835, 2013, Volume 329, Issue 1, pp. 9 - 16
Highlights ► Lipophilic statin, simvastatin, triggers apoptosis in human breast cancer cells via JNK/CHOP/DR5 dependent signaling. ► Simvastatin blockage of... 
Hematology, Oncology and Palliative Medicine | c-Jun N-terminal kinase (JNK) | Simvastatin (SVA) | CCAAT/enhancer binding protein homologous protein (CHOP) | Death receptor-5 (DR5) | Human breast cancer cells | Apoptosis | C-Jun N-terminal kinase (JNK) | DOWN-REGULATION | CYCLE ARREST | homologous protein (CHOP) | DEATH | ENDOPLASMIC-RETICULUM STRESS | INDUCTION | CCAAT/enhancer binding protein | COLON-CANCER | ONCOLOGY | GROWTH | NF-KAPPA-B | EXPRESSION | MOLECULAR-MECHANISMS | Transcription Factor CHOP - genetics | Apoptosis - drug effects | Humans | JNK Mitogen-Activated Protein Kinases - metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism | Mevalonic Acid - metabolism | Simvastatin - pharmacology | Breast Neoplasms - drug therapy | Breast Neoplasms - metabolism | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | MAP Kinase Signaling System - drug effects | Signal Transduction - drug effects | Breast Neoplasms - pathology | Cell Line, Tumor | Female | Antineoplastic Agents - pharmacology | Polyisoprenyl Phosphates - pharmacology | RNA, Small Interfering | Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics | JNK Mitogen-Activated Protein Kinases - genetics | Sesquiterpenes - pharmacology | Transcription Factor CHOP - metabolism | Phosphates | Simvastatin | Cancer cells | Breast cancer | Protein binding | Antilipemic agents
Journal Article
Molecular cancer therapeutics, ISSN 1538-8514, 2009, Volume 8, Issue 2, pp. 449 - 457
Differentiation is a complex set of events that can be blocked by rearrangements of regulatory genes producing fusion proteins with altered properties. In the... 
C/EBP | Transcription | Sarcoma | Trabectedin | Adipogenesis | ACTIVATION | ONCOLOGY | ECTEINASCIDIN-743 | TRANSCRIPTION | GENE-EXPRESSION | ADIPOCYTE DIFFERENTIATION | FUS/TLS-CHOP | NUCLEOTIDE-EXCISION | DNA-REPAIR PATHWAYS | CHOP FUSION PROTEIN | BINDING-PROTEINS | Tetrahydroisoquinolines - pharmacology | Transcription Factor CHOP - genetics | Apoptosis - drug effects | Adipogenesis - drug effects | Humans | Middle Aged | Liposarcoma, Myxoid - pathology | RNA-Binding Protein FUS - genetics | Male | CCAAT-Enhancer-Binding Protein-beta - metabolism | Cell Differentiation - drug effects | Oncogene Proteins, Fusion - genetics | Protein Binding - drug effects | Biomarkers, Tumor - metabolism | Cell Line, Tumor | Dioxoles - pharmacology | Female | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Liposarcoma, Myxoid - genetics | Adipogenesis - genetics | Drug Screening Assays, Antitumor | pathology | CCAAT-Enhancer-Binding Protein-beta | Oncogene Proteins | Tumor Markers | genetics | Transcription Factor CHOP | Surgery | pharmacology | Antitumor | Myxoid | Tumor | Cell Differentiation | Tetrahydroisoquinolines | Cell Line | Gene Expression Regulation | Antineoplastic Agents | drug effects | Biological | Kirurgi | Dioxoles | Drug Screening Assays | Liposarcoma | Protein Binding | metabolism | RNA-Binding Protein FUS | Cancer and Oncology | Neoplastic | Fusion | Cancer och onkologi | Apoptosis
Journal Article
Journal of pediatric gastroenterology and nutrition, ISSN 0277-2116, 2011, Volume 53, Issue 2, pp. 1 - 140
ABSTRACTWith the epidemic of childhood obesity, nonalcoholic fatty liver disease (NAFLD) has become the most common cause of chronic liver disease in... 
nonalcoholic steatohepatitis | nonalcoholic fatty liver disease | C/EBP-homologous protein (CHOP) | free fatty acids | Bcl-2 homology 3-only protein | c-Jun-N-terminal kinase | endoplasmic reticulum stress | INDUCED NONALCOHOLIC STEATOHEPATITIS | 3 GENE PNPLA3 | FATTY LIVER-DISEASE | ENDOPLASMIC-RETICULUM STRESS | CELL-DEATH | HEPATOCYTE LIPOAPOPTOSIS | NUTRITION & DIETETICS | UNFOLDED PROTEIN RESPONSE | INSULIN-RESISTANCE | PEDIATRICS | GASTROENTEROLOGY & HEPATOLOGY | HEPATIC STEATOSIS | C/EBP-HOMOLOGOUS PROTEIN | Dietary Fats - metabolism | Obesity - drug therapy | Apoptosis - drug effects | Humans | JNK Mitogen-Activated Protein Kinases - metabolism | Molecular Targeted Therapy | Adipose Tissue - metabolism | Adult | Child | Dietary Fats - adverse effects | Fatty Liver - metabolism | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Endoplasmic Reticulum Stress - drug effects | Fatty Liver - physiopathology | Obesity - physiopathology | Transcription Factor CHOP - antagonists & inhibitors | Fatty Liver - drug therapy | Apoptosis Regulatory Proteins - metabolism | Obesity - metabolism | Animals | Adolescent | Apoptosis Regulatory Proteins - antagonists & inhibitors | Lipid Metabolism - drug effects | Transcription Factor CHOP - metabolism | Adipose Tissue - drug effects | Fatty Liver - etiology | Index Medicus | Bcl-2 homology 3 (BH3)-only protein | lipoapoptosis | nonalcoholic steatohepatitis (NASH) | EBP-homologous protein (CHOP) | nonalcoholic fatty liver disease (NAFLD) | c-Jun-N-terminal kinase (JNK) | endoplasmic reticulum (ER) stress | free fatty acids (FFA)s
Journal Article
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2017, Volume 114, Issue 29, pp. E5805 - E5814
Journal Article
Journal Article
Journal of Hepatology, ISSN 0168-8278, 2013, Volume 59, Issue 3, pp. 495 - 503
Journal Article