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American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 10/2008, Volume 178, Issue 8, pp. 838 - 846
Rationale The molecular pathomechanisms underlying idiopathic pulmonary fibrosis (IPF) are elusive, but chronic epithelial injury has recently been suggested... 
C/EBP-homologous protein | X-box binding protein-1 | Type II alveolar epithelial cell | Interstitial lung disease | Lung fibrosis | LUNG | OXIDATIVE STRESS | ACTIVATION | INTERSTITIAL PNEUMONIA | lung fibrosis | CELL-DEATH | PATHOGENESIS | UNFOLDED PROTEIN RESPONSE | interstitial lung disease | RESPIRATORY SYSTEM | CHOP | MYOFIBROBLASTS | MUTATIONS | type II alveolar epithelial cell | CRITICAL CARE MEDICINE | Immunohistochemistry | Humans | Middle Aged | Oxidative Stress - physiology | Endoplasmic Reticulum - metabolism | Male | Pulmonary Fibrosis - genetics | Pulmonary Disease, Chronic Obstructive - pathology | Activating Transcription Factor 6 - genetics | X-Box Binding Protein 1 | RNA - genetics | Activating Transcription Factor 6 - biosynthesis | Endoplasmic Reticulum - pathology | Pulmonary Alveoli - metabolism | Female | Pulmonary Fibrosis - metabolism | Pulmonary Disease, Chronic Obstructive - metabolism | Pulmonary Disease, Chronic Obstructive - genetics | In Situ Nick-End Labeling | Severity of Illness Index | Gene Expression | Pulmonary Alveoli - pathology | Activating Transcription Factor 4 - genetics | Transcription Factors - biosynthesis | Pulmonary Fibrosis - pathology | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Regulatory Factor X Transcription Factors | Blotting, Western | Activating Transcription Factor 4 - biosynthesis | Apoptosis - physiology | DNA-Binding Proteins - biosynthesis | EBP-homologous protein | E. Interstitial Lung Disease
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 10/2010, Volume 285, Issue 43, pp. 33165 - 33174
In response to different environmental stresses, phosphorylation of eIF2 (eIF2 similar to P) represses global translation coincident with preferential... 
GCN2 | OXIDATIVE STRESS | UNFOLDED PROTEIN RESPONSE | HEPATITIS-C VIRUS | EIF2-ALPHA KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENE-EXPRESSION | EUKARYOTIC INITIATION-FACTOR-2 | ENDOPLASMIC-RETICULUM STRESS | NF-KAPPA-B | MAMMALIAN-CELLS | Transcription Factor CHOP - genetics | Apoptosis - radiation effects | Humans | Protein Biosynthesis - physiology | Transcription, Genetic - radiation effects | Unfolded Protein Response - radiation effects | Endoplasmic Reticulum - metabolism | Stress, Physiological - radiation effects | RNA, Messenger - biosynthesis | Ultraviolet Rays | Eukaryotic Initiation Factor-2 - metabolism | Protein Biosynthesis - radiation effects | Stress, Physiological - physiology | Endoplasmic Reticulum - genetics | Cell Survival | RNA, Messenger - genetics | Activating Transcription Factor 4 - genetics | Gene Expression Regulation - physiology | Mice, Knockout | Transcription, Genetic - physiology | Animals | Eukaryotic Initiation Factor-2 - genetics | Activating Transcription Factor 4 - biosynthesis | Cell Line, Tumor | Gene Expression Regulation - radiation effects | Mice | Apoptosis - physiology | Transcription Factor CHOP - metabolism | Unfolded Protein Response - physiology | Index Medicus | Gene Regulation | Gene Expression | Translation | Integrated Stress Response | Protein Synthesis | ER Stress | Translation Regulation | Protein Synthesis and Degradation | eIF2 Kinase | Translation Control | Translation Initiation Factors
Journal Article
Cancer Research, ISSN 0008-5472, 02/2007, Volume 67, Issue 3, pp. 1262 - 1269
Journal Article
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 2015, Volume 308, Issue 8, pp. C621 - C630
Premature senescence is an important event during diabetic nephropathy (DN) progression. Here, we investigated the role of endoplasmic reticulum (ER)... 
Advanced glycation end products | Premature senescence | Activating transcription factor 4 | Endoplasmic reticulum stress | PHYSIOLOGY | PHOSPHORYLATION | ENDOPLASMIC-RETICULUM STRESS | advanced glycation end products | CELLULAR SENESCENCE | premature senescence | endoplasmic reticulum stress | CELL BIOLOGY | p16 | PATHWAY | ACCELERATED SENESCENCE | DIFFERENTIATION | KIDNEY | EXPRESSION | PROGRESSION | activating transcription factor 4 | GLYCATION END-PRODUCTS | Humans | Middle Aged | Heat-Shock Proteins - biosynthesis | Male | Neoplasm Proteins - metabolism | Cadherins - biosynthesis | Cyclin-Dependent Kinase Inhibitor p16 | Endoplasmic Reticulum - pathology | RNA Interference | Cellular Senescence | Female | Epithelial Cells - cytology | Neoplasm Proteins - genetics | Aging, Premature - metabolism | Diabetic Nephropathies - pathology | Endoplasmic Reticulum Stress - drug effects | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Cells, Cultured | Activating Transcription Factor 4 - genetics | Kidney Tubules - cytology | Animals | Activating Transcription Factor 4 - metabolism | Glycation End Products, Advanced - metabolism | Activating Transcription Factor 4 - biosynthesis | Aged | Mice | RNA, Small Interfering | Endoplasmic Reticulum Stress - physiology | Development and progression | Genetic aspects | Cellular signal transduction | Epithelium | Health aspects | Diabetic nephropathies
Journal Article
Cellular Signalling, ISSN 0898-6568, 03/2014, Volume 26, Issue 3, pp. 556 - 563
Histone deacetylase 4 (HDAC4) is involved in the regulation of many fundamental cell processes such as proliferation, differentiation, and survival via the... 
HDAC4 | Cell apoptosis | Endoplasmic reticulum stress | ATF4 | HISTONE DEACETYLASE 4 | DEATH | ENDOPLASMIC-RETICULUM STRESS | ACTIVATING TRANSCRIPTION FACTOR-4 | AUTOPHAGY | PERK | CELL BIOLOGY | CREB2 | GROWTH | NEURONS | BINDING | Calcium-Transporting ATPases - antagonists & inhibitors | Up-Regulation | Phosphorylation | Transcriptional Activation - genetics | Histone Deacetylases - biosynthesis | eIF-2 Kinase - metabolism | Humans | Endoplasmic Reticulum - metabolism | Apoptosis - genetics | Endoplasmic Reticulum Stress - genetics | Glycosylation - drug effects | RNA Interference | HEK293 Cells | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Eukaryotic Initiation Factor-2 - metabolism | Transcription Factor CHOP - biosynthesis | Repressor Proteins - metabolism | Cell Line | Endoplasmic Reticulum Stress - drug effects | Histone Deacetylases - genetics | Signal Transduction | eIF-2 Kinase - biosynthesis | Enzyme Inhibitors - pharmacology | Activating Transcription Factor 4 - genetics | Repressor Proteins - genetics | Histone Deacetylases - metabolism | Cell Cycle Proteins - biosynthesis | Protein-Serine-Threonine Kinases - biosynthesis | Animals | Repressor Proteins - biosynthesis | Activating Transcription Factor 4 - metabolism | Activating Transcription Factor 4 - biosynthesis | Thapsigargin - pharmacology | Mice | RNA, Small Interfering | Transcription, Genetic - genetics | 3T3 Cells | Apoptosis | Stresses | Control | Genes | Histones | Differentiation | Survival | Cytoplasm
Journal Article
Plant Biotechnology Journal, ISSN 1467-7644, 10/2017, Volume 15, Issue 10, pp. 1284 - 1294
The overexpression of miR319 in plants results in delayed senescence, and high levels of miR319‐targeted TCP4 transcription factor cause premature onset of... 
Plants (botany) | Senescence | Cell activation | Transcription factors | Cell death | Cell walls | Switches | Abundance | Biosynthesis | Apoptosis
Journal Article
Immunity, ISSN 1074-7613, 04/2018, Volume 48, Issue 4, pp. 730 - 744.e5
Although characterization of T cell exhaustion has unlocked powerful immunotherapies, the mechanisms sustaining adaptations of short-lived innate cells to... 
type I interferon | plasmacytoid dendritic cells | chronic viral infection | LCMV | HIV | exhaustion | cancer | TLR | ACTIVATION | CONTRIBUTE | MURINE CYTOMEGALOVIRUS-INFECTION | HIV-INFECTION | ALPHA PRODUCTION | INNATE | IMMUNOLOGY | HEPATITIS-B | LYMPHOCYTIC CHORIOMENINGITIS VIRUS | TRANSCRIPTION FACTOR E2-2 | I INTERFERON RESPONSES | Cell Self Renewal - immunology | Lymphocytic choriomeningitis virus - immunology | Cell Line | Cell Proliferation | Carrier Proteins - biosynthesis | Dendritic Cells - immunology | Humans | Mice, Inbred C57BL | Transcription Factors - biosynthesis | Inflammation - immunology | Interferon Type I - immunology | Lymphocytic Choriomeningitis - immunology | Mice, Knockout | Signal Transduction - immunology | Animals | Nuclear Proteins - biosynthesis | Toll-Like Receptor 7 - immunology | Transcription Factor 4 - biosynthesis | Dendritic Cells - cytology | Mice | Membrane Glycoproteins - immunology | DNA-Binding Proteins - biosynthesis | 3T3 Cells | Medical research | Dendritic cells | Immunotherapy | Medicine, Experimental | Cytomegalovirus infections | Fatigue | Interferon | Biological response modifiers | T cells | Immunoglobulin A | Health aspects | Adaptations | Flow cytometry | Chronic infection | Viruses | Infections | Lymphocytes T | Experiments | Design | Rodents | Bone marrow | Toll-like receptors | Tumor necrosis factor-TNF | Spleen | Pathogens | TLR7 protein | Inflammation | CD4 antigen | Human subjects | Exhaustion | Secondary infection | Production capacity | Viral infections | Cancer | Type I interferon
Journal Article
Journal Article
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