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The Journal of biological chemistry, ISSN 0021-9258, 2018, Volume 293, Issue 44, pp. 17008 - 17020
.... Here, using mouse models of CKD, we 1) studied the contribution of the proapoptotic transcription factor CCAAT enhancer-binding protein homologous protein (CHOP... 
vascular calcification | fatty acid | cyclin-dependent kinase (CDK) | kidney disease | vascular biology | ENDOPLASMIC-RETICULUM STRESS | SMOOTH-MUSCLE | IN-VITRO | GENE-EXPRESSION | CHOP | saturated fatty acids | vascular smooth muscle cells | atherosclerosis | RNA-POLYMERASE-II | MAMMALIAN TARGET | cardiovascular disease | BIOCHEMISTRY & MOLECULAR BIOLOGY | ER stress | endoplasmic reticulum stress (ER stress) | renal dysfunction | P-TEFB | CDK9 | ARTERIAL CALCIFICATION | CHRONIC KIDNEY-DISEASE | CELL-DIFFERENTIATION | Transcription Factor CHOP - genetics | Phosphorylation | Cyclin T - metabolism | Humans | Vascular Calcification - genetics | Male | Renal Insufficiency, Chronic - complications | Renal Insufficiency, Chronic - metabolism | Vascular Calcification - metabolism | Vascular Calcification - etiology | Renal Insufficiency, Chronic - genetics | Vascular Calcification - physiopathology | Mice, Inbred DBA | Fatty Acids - metabolism | Myocytes, Smooth Muscle - metabolism | Cyclin-Dependent Kinase 9 - genetics | Cyclin T - genetics | Activating Transcription Factor 4 - genetics | Mice, Transgenic | Renal Insufficiency, Chronic - physiopathology | Animals | Activating Transcription Factor 4 - metabolism | Endoplasmic Reticulum Stress | Protein Binding | Cyclin-Dependent Kinase 9 - metabolism | Mice | Transcription Factor CHOP - metabolism | Lipids
Journal Article
American journal of physiology: Gastrointestinal and liver physiology, ISSN 1522-1547, 2010, Volume 299, Issue 1, pp. G236 - G243
... (p53 upregulated modulator of apoptosis). Although the activator protein (AP)-1 complex facilitates PUMA expression by saturated FFA, the transcription factor CAAT/enhancer binding homologous protein (CHOP... 
c-Jun | Activator protein-1 | p53 upregulated modulator of apoptosis | Nonalcoholic steatohepatitis | CAAT/enhancer binding homologous protein | BH3-only proteins | Hepatic steatosis | Endoplasmic reticulum stress | ACTIVATION | HEPATOCYTES | PHYSIOLOGY | PROTEIN | INDUCED APOPTOSIS | activator protein-1 | ER STRESS | ENDOPLASMIC-RETICULUM STRESS | endoplasmic reticulum stress | hepatic steatosis | CELL-DEATH | FAMILY | nonalcoholic steatohepatitis | BAX | GASTROENTEROLOGY & HEPATOLOGY | Palmitic Acid - metabolism | Transcription Factor CHOP - genetics | Up-Regulation | Phosphorylation | Fatty Liver - pathology | Transcription Factor AP-1 - genetics | Humans | Transcriptional Activation | Endoplasmic Reticulum - metabolism | Hepatocytes - pathology | Hepatocytes - metabolism | RNA, Messenger - metabolism | Transcription Factor AP-1 - metabolism | Transfection | RNA Interference | Apoptosis Regulatory Proteins - genetics | Binding Sites | Fatty Liver - genetics | Proto-Oncogene Proteins - metabolism | Promoter Regions, Genetic | Oleic Acid - metabolism | Fatty Liver - metabolism | bcl-2-Associated X Protein - metabolism | Proto-Oncogene Proteins - genetics | Apoptosis Regulatory Proteins - metabolism | Proto-Oncogene Proteins c-jun - metabolism | Cell Line, Tumor | Transcription Factor CHOP - metabolism | Apoptosis | Physiological aspects | Genetic aspects | Gene expression | Binding proteins | Properties | Endoplasmic reticulum | enhancer binding homologous protein | Liver and Biliary Tract | CAAT
Journal Article
Journal Article
PloS one, ISSN 1932-6203, 2012, Volume 7, Issue 6, p. e39586
... death, independent of p53. CHOP (C/EBP homologous protein also known as GADD153; gene name Ddit3), a critical initiator of ER stress-induced apoptosis, was found... 
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
Cancer Science, ISSN 1347-9032, 05/2014, Volume 105, Issue 5, pp. 520 - 527
Although tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) has shown efficacy in a phase 2 clinical trial, development of resistance to TRAIL by tumor cells is a major roadblock... 
quercetin | CCAAT enhancer‐binding protein homologous protein | tumor necrosis factor‐related apoptosis‐inducing ligand | death receptor 5 | reactive oxygen species | Death receptor 5 | Reactive oxygen species | Tumor necrosis factor-related apoptosis-inducing ligand | CCAAT enhancer-binding protein homologous protein | Quercetin | CARCINOMA-CELLS | DOWN-REGULATION | DEATH | ENDOPLASMIC-RETICULUM STRESS | ONCOLOGY | RESISTANCE | tumor necrosis factor-related apoptosis-inducing ligand | CHOP | CASPASE-8 | DR5 UP-REGULATION | EXPRESSION | MODULATION | Transcription Factor CHOP - genetics | Up-Regulation | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Humans | Caspase 3 - metabolism | JNK Mitogen-Activated Protein Kinases - metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand - biosynthesis | DNA-Binding Proteins - metabolism | TNF-Related Apoptosis-Inducing Ligand - pharmacology | RNA Interference | Membrane Potential, Mitochondrial | Female | Ovarian Neoplasms - drug therapy | Promoter Regions, Genetic | Endoplasmic Reticulum Stress - drug effects | Quercetin - therapeutic use | Antioxidants - pharmacology | TNF-Related Apoptosis-Inducing Ligand - metabolism | Xenograft Model Antitumor Assays | Antioxidants - therapeutic use | Animals | Quercetin - pharmacology | Mice, Nude | Cell Line, Tumor | Mice | RNA, Small Interfering | Enzyme Activation | Transcription Factor CHOP - metabolism | Transcription factors | Oxygen | Cell survival | Tumor cells | Caspase | Kinases | Cancer therapies | Ovarian cancer | Proteins | Studies | Signal transduction | Flavonoids | Tumor necrosis factor | Cell death | Natural products | Xenografts | Tumor necrosis factor-TNF | Ligands | TRAIL protein | Endoplasmic reticulum | Apoptosis | Original
Journal Article
Experimental cell research, ISSN 0014-4827, 2011, Volume 317, Issue 11, pp. 1621 - 1628
Journal Article
Cell death and differentiation, ISSN 1350-9047, 11/2012, Volume 19, Issue 11, pp. 1836 - 1846
Induction of the C/EBP homologous protein (CHOP) is considered a key event for endoplasmic reticulum (ER... 
ER stress | apoptosis | CHOP | Bcl-2 proteins | inflammation | pancreatic b-cell | OXIDATIVE STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOWN-REGULATION | NECROSIS-FACTOR-ALPHA | DEATH | ENDOPLASMIC-RETICULUM STRESS | INDUCTION | CELL BIOLOGY | pancreatic beta-cell | INSULIN-PRODUCING CELLS | GENE-EXPRESSION | NF-KAPPA-B | POSTTRANSLATIONAL MODIFICATION | Transcription Factor CHOP - genetics | Interleukin-1beta - pharmacology | Caspase 9 - metabolism | Apoptosis - drug effects | Caspase 3 - metabolism | Diabetes Mellitus, Type 1 - metabolism | NF-kappa B - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Insulin-Secreting Cells - metabolism | Cell Nucleus - metabolism | I-kappa B Kinase - metabolism | Insulin-Secreting Cells - cytology | Cell Line | Diabetes Mellitus, Type 1 - pathology | Rats | Transcription Factor CHOP - antagonists & inhibitors | Mitochondria - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Animals | Transcription Factor RelA - metabolism | Endoplasmic Reticulum Stress | Myeloid Cell Leukemia Sequence 1 Protein | Transcription Factor CHOP - metabolism | Cytokines - pharmacology | Interferon-gamma - pharmacology | Insulitis | Transcription factors | Fas antigen | Bcl-2 protein | Leukocytes (mononuclear) | CCAAT/enhancer-binding protein | Mitochondria | Pancreas | Cytokines | CD95 antigen | Diabetes mellitus | Data processing | Inflammation | Interleukin 15 | Mcl-1 protein | Nitric-oxide synthase | Nuclear transport | Stress | Beta cells | Interferon regulatory factor 7 | NF- Kappa B protein | CXCL10 protein | Caspase-9 | Islets of Langerhans | Endoplasmic reticulum | Chemokines | Apoptosis | B-cell lymphoma | Original Paper | pancreatic β-cell
Journal Article
Journal of Hepatology, ISSN 0168-8278, 2013, Volume 59, Issue 3, pp. 495 - 503
Journal Article