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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
Nature immunology, ISSN 1529-2916, 2010, Volume 11, Issue 5, pp. 411 - 418
.... and its downstream target, the transcription factor XBP1. Previously described ER-stress target genes of XBP1 were not induced by TLR signaling... 
UNFOLDED PROTEIN RESPONSE | PATHWAY | ER STRESS | HOST-DEFENSE | ENDOPLASMIC-RETICULUM STRESS | FRANCISELLA-TULARENSIS INFECTION | IMMUNOLOGY | LIVE VACCINE STRAIN | INFLAMMATORY RESPONSE | NEGATIVE REGULATOR | SYSTEMS BIOLOGY | RNA, Small Interfering - genetics | Endoribonucleases - genetics | Tularemia - metabolism | Toll-Like Receptor 2 - genetics | Membrane Glycoproteins - metabolism | Lipopeptides - pharmacology | Transcriptional Activation - drug effects | NADPH Oxidases - metabolism | Tularemia - genetics | Protein Splicing - genetics | Transcriptional Activation - immunology | X-Box Binding Protein 1 | Protein Splicing - drug effects | NADPH Oxidases - genetics | Stress, Physiological - drug effects | TNF Receptor-Associated Factor 6 - genetics | Transcription Factor CHOP - biosynthesis | Transcription Factors - immunology | Cytokines - genetics | Protein-Serine-Threonine Kinases - metabolism | DNA-Binding Proteins - immunology | Endoribonucleases - metabolism | Macrophages - pathology | Stress, Physiological - genetics | Myeloid Differentiation Factor 88 - genetics | Toll-Like Receptor 4 - genetics | Signal Transduction - genetics | Toll-Like Receptor 4 - immunology | Toll-Like Receptor 2 - metabolism | Toll-Like Receptor 4 - metabolism | Mice, Knockout | Macrophages - metabolism | Signal Transduction - drug effects | Tunicamycin - pharmacology | Lipopolysaccharides - pharmacology | Toll-Like Receptor 2 - immunology | Mice | Stress, Physiological - immunology | Endoribonucleases - immunology | Transcription Factor CHOP - genetics | NADPH Oxidases - immunology | DNA-Binding Proteins - metabolism | Signal Transduction - immunology | Macrophages - virology | Mice, Mutant Strains | Tularemia - immunology | Membrane Glycoproteins - immunology | Macrophages - immunology | Cytokines - immunology | Cell Line | Francisella tularensis - immunology | Protein Splicing - immunology | Protein-Serine-Threonine Kinases - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Immunity, Innate | NADPH Oxidase 2 | Regulatory Factor X Transcription Factors | Mice, Inbred C3H | Membrane Glycoproteins - genetics | Transcription Factors - metabolism | Animals | TNF Receptor-Associated Factor 6 - metabolism | Macrophages - drug effects | Protein-Serine-Threonine Kinases - immunology | Francisella tularensis - pathogenicity | Myeloid Differentiation Factor 88 - metabolism | Cytokines - biosynthesis | Cell receptors | Transcription factors | Immune response | Physiological aspects | Genetic aspects | Research | Health aspects | Francisella tularensis
Journal Article
Journal Article
The EMBO journal, ISSN 1460-2075, 2005, Volume 24, Issue 6, pp. 1243 - 1255
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
Journal Article
Experimental cell research, ISSN 0014-4827, 2011, Volume 317, Issue 11, pp. 1621 - 1628
Journal Article
PloS one, ISSN 1932-6203, 2012, Volume 7, Issue 4, p. e33208
DDIT3, also known as GADD153 or CHOP, encodes a basic leucine zipper transcription factor of the dimer forming C/EBP family... 
TRANSCRIPTION FACTOR CHOP | IN-VITRO | MYXOID LIPOSARCOMA | INDUCED APOPTOSIS | BIOLOGY | BINDING-PROTEIN | GENE-EXPRESSION | PANCREATIC BETA-CELLS | ENDOPLASMIC-RETICULUM STRESS | AMINO-ACID LIMITATION | C/EBP-HOMOLOGOUS PROTEIN | Transcription Factor CHOP - genetics | Cell Proliferation | Oligonucleotide Array Sequence Analysis | Humans | Cytoplasm - metabolism | Gene Expression Profiling | Green Fluorescent Proteins - genetics | Fibrosarcoma - metabolism | Promoter Regions, Genetic - genetics | Liposarcoma - metabolism | Cell Nucleus - metabolism | Flow Cytometry | Biomarkers, Tumor - metabolism | Real-Time Polymerase Chain Reaction | Fibroblasts - metabolism | Recombinant Proteins - metabolism | Antineoplastic Agents, Hormonal - pharmacology | Liposarcoma - drug therapy | RNA, Messenger - genetics | Cells, Cultured | Liposarcoma - genetics | Recombinant Proteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Cell Adhesion | Blotting, Western | Fibrosarcoma - genetics | Cell Cycle | Cell Nucleus - genetics | Fibroblasts - drug effects | Tamoxifen - pharmacology | Biomarkers, Tumor - genetics | Fibroblasts - cytology | Cell Nucleus - drug effects | Transcription Factor CHOP - metabolism | Cytoplasm - drug effects | Fibrosarcoma - drug therapy | Cell Movement | Genomes | Genetic transcription | DNA binding proteins | Tamoxifen | Genes | Genomics | Cell culture | Transcription factors | Target recognition | Amino acids | Biochemistry | CCAAT/enhancer-binding protein | Leucine | Kinases | Experiments | Proteins | Cell growth | Annotations | Cell cycle | Fibroblasts | Physiology | Localization | Stress response | Deoxyribonucleic acid--DNA | Translocation | Stresses | Cell survival | Cloning | Forming | Gene expression | Stress | Nuclear transport | Leucine zipper proteins | Pathology | DNA microarrays | Ligands | Prostate | Cell migration | CHOP protein | Cellular stress response | Apoptosis | Cancer | cytology | Green Fluorescent Proteins | RNA | Hormonal | Genetic | Fibrosarcoma | Recombinant Proteins | Blotting | Tumor Markers | Western | genetics | Transcription Factor CHOP | pharmacology | Cultured | drug therapy | Promoter Regions | Antineoplastic Agents | drug effects | Messenger | Biological | Cells | Liposarcoma | metabolism | Cancer and Oncology | Cell Nucleus | Cytoplasm | Cancer och onkologi | Deoxyribonucleic acid | DNA
Journal Article
Journal Article