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Nature, ISSN 0028-0836, 11/2009, Volume 462, Issue 7269, pp. 99 - 103
Journal Article
Cancer Letters, ISSN 0304-3835, 05/2017, Volume 394, pp. 22 - 32
Hepatitis B virus X protein (HBx) plays an important role in the progression of hepatocellular carcinoma. Here we reported that overexpression of HBx in... 
High mobility group box 1 | Calmodulin dependent protein kinase | Hepatocellular carcinoma | Metastasis | Hepatitis B virus X protein | CELLS | DNA-BINDING | PHOSPHATIDYLINOSITOL 3-KINASE | HMGB1 | RELEASE | HBX PROTEIN | LIVER-CANCER | IN-VITRO | ONCOLOGY | NUCLEAR FACTOR | NF-KAPPA-B | Hepatitis B - metabolism | Hepatitis B - genetics | Humans | Lung Neoplasms - metabolism | Middle Aged | Hepatitis B - virology | Male | Antineoplastic Agents - therapeutic use | Viral Load | Hepatitis B - complications | Time Factors | HMGB1 Protein - metabolism | Liver Neoplasms - pathology | Calcium Chelating Agents - pharmacology | HMGB1 Protein - antagonists & inhibitors | Liver Neoplasms - virology | Carcinoma, Hepatocellular - virology | Host-Pathogen Interactions | Calcium-Calmodulin-Dependent Protein Kinase Type 4 - antagonists & inhibitors | Cell Movement - drug effects | Lung Neoplasms - prevention & control | Gene Expression Regulation, Viral | Hepatitis B virus - genetics | Liver Neoplasms - metabolism | Cell Line, Tumor | Mice, Inbred NOD | Hepatitis B virus - metabolism | DNA, Viral - genetics | Carcinoma, Hepatocellular - metabolism | Prognosis | Calcium-Calmodulin-Dependent Protein Kinase Type 4 - metabolism | Carcinoma, Hepatocellular - secondary | Liver Neoplasms - therapy | Transfection | Lung Neoplasms - secondary | Trans-Activators - genetics | Female | Calcium Signaling | Proportional Hazards Models | Lung Neoplasms - virology | Mice, SCID | Antibodies - pharmacology | Xenograft Model Antitumor Assays | Animals | Calcium-Calmodulin-Dependent Protein Kinase Kinase - antagonists & inhibitors | Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism | Trans-Activators - metabolism | Carcinoma, Hepatocellular - therapy | Protein Kinase Inhibitors - pharmacology | Medical colleges | Chromosomal proteins | Liver | Antibodies | Development and progression | Hepatoma | Viral antibodies | International cooperation | Analysis | Cellular signal transduction | Hepatitis B virus | Health aspects | Hepatitis B | Protein kinases | Calmodulin | Cell culture | Transcription factors | Ca2+/calmodulin-dependent protein kinase IV | Error analysis | Bcl-2 protein | Mobility | AKT protein | Mesothelioma | Biochemistry | ADP | Risk factors | Metastases | Proteins | Liver cancer | Hepatitis | Signal transduction | Cell activation | Ischemia | Surgery | Membrane potential | Deoxyribonucleic acid--DNA | Binding | Liver diseases | Biochemical analysis | Mortality | Activator protein 1 | Hazards | Regression analysis | Gene expression | Survival | 1-Phosphatidylinositol 3-kinase | Hypoxia | Viability | Biotechnology | Calcium | Viruses | Stimulation | Infections | Activation | Kinases | DNA repair | Carcinogenesis | Rodents | Bacteria | Calcium (intracellular) | Statistical analysis | Invasiveness | Tumor cells | Markers | Inflammation | Permeability | Computer programs | Cell death | Medical prognosis | Bcl protein | In vivo methods and tests | Cytoplasm | Apoptosis | Cancer | Index Medicus
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 01/2014, Volume 21, Issue 1, pp. 79 - 91
The immunogenic demise of cancer cells can be induced by various chemotherapeutics, such as anthracyclines and oxaliplatin, and provokes an immune response... 
quinacrine | apoptosis | U2OS cells | caspases | endoplasmic reticulum stress | Beclin 1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | RELEASE | AUTOPHAGY | CLEAVAGE | CHEMOTHERAPY | CELL BIOLOGY | CALRETICULIN EXPOSURE | PANNEXIN 1 | ASSAYS | FIND-ME SIGNAL | Connexins - antagonists & inhibitors | RNA-Binding Proteins - genetics | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Humans | Cell Death - immunology | rho-Associated Kinases - antagonists & inhibitors | Antineoplastic Agents - toxicity | DNA-Binding Proteins - metabolism | Lysosomes - metabolism | Lysosomal-Associated Membrane Protein 1 - genetics | Myosin Type II - metabolism | RNA Interference | rho-Associated Kinases - metabolism | Adenosine Triphosphate - metabolism | HMGB1 Protein - metabolism | Cell Membrane - metabolism | Cell Death - drug effects | RNA-Binding Proteins - antagonists & inhibitors | Nerve Tissue Proteins - antagonists & inhibitors | DNA-Binding Proteins - antagonists & inhibitors | Connexins - genetics | rho-Associated Kinases - genetics | Lysosomal-Associated Membrane Protein 1 - antagonists & inhibitors | Microtubule-Associated Proteins - antagonists & inhibitors | DNA-Binding Proteins - genetics | Nerve Tissue Proteins - genetics | Connexins - metabolism | Nerve Tissue Proteins - metabolism | Animals | Autophagy-Related Protein 5 | Cell Line, Tumor | Lysosomal-Associated Membrane Protein 1 - metabolism | Mice | RNA-Binding Proteins - metabolism | RNA, Small Interfering - metabolism | Index Medicus | Original Paper
Journal Article
Journal Article
Nature Communications, ISSN 2041-1723, 10/2016, Volume 7, Issue 1, pp. 13280 - 13280
Sepsis, severe sepsis and septic shock are the main cause of mortality in non-cardiac intensive care units. Immunometabolism has been linked to sepsis;... 
IL-1-BETA PRODUCTION | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | PYRUVATE-KINASE M2 | LACTATE | HMGB1 RELEASE | SEPTIC SHOCK | INTRACELLULAR LPS | SEPSIS | PKR ACTIVATION | INNATE IMMUNITY | Interleukin-18 - immunology | Phosphorylation | eIF-2 Kinase - metabolism | Humans | Male | HMGB1 Protein - immunology | HMGB1 Protein - secretion | DNA-Binding Proteins - metabolism | Signal Transduction - immunology | Macrophages - secretion | Female | Membrane Proteins - metabolism | Carrier Proteins - immunology | Macrophages - immunology | Disease Models, Animal | eIF-2 Kinase - genetics | Interleukin-1beta - secretion | Sepsis - immunology | DNA-Binding Proteins - immunology | Membrane Proteins - genetics | NLR Family, Pyrin Domain-Containing 3 Protein - metabolism | Coinfection - immunology | Carrier Proteins - antagonists & inhibitors | Interleukin-1beta - immunology | Membrane Proteins - immunology | Naphthoquinones - pharmacology | Thyroid Hormones - genetics | eIF-2 Kinase - antagonists & inhibitors | Mice, Knockout | Thyroid Hormones - immunology | Carrier Proteins - genetics | Coinfection - microbiology | Macrophages - metabolism | Animals | Carrier Proteins - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein - immunology | Membrane Proteins - antagonists & inhibitors | Thyroid Hormones - metabolism | Inflammasomes - immunology | Myeloid Cells - metabolism | Interleukin-18 - secretion | Mice | Mice, Inbred BALB C | Glycolysis - immunology | Sepsis - microbiology | Index Medicus
Journal Article
Microvascular Research, ISSN 0026-2862, 2011, Volume 81, Issue 2, pp. 189 - 197
Acute lung injury (ALI) results from loss of alveolar-capillary barrier integrity and the evolution of high-permeability pulmonary edema resulting in alveolar... 
Acute lung injury | MAP kinase | HMGB1 | RAGE | Hsp27 | Endothelium | ACTIVATION | PERMEABILITY | HEAT-SHOCK PROTEIN-27 | RECEPTOR | GROUP BOX-1 PROTEIN | RESPIRATORY-DISTRESS-SYNDROME | P38 MAP KINASE | TUMOR-NECROSIS-FACTOR | PERIPHERAL VASCULAR DISEASE | DYSFUNCTION | GLYCATION END-PRODUCTS | Capillary Permeability - physiology | RNA, Small Interfering - genetics | Cadherins - metabolism | Stress Fibers - drug effects | Humans | Actins - metabolism | Capillary Permeability - drug effects | Intracellular Signaling Peptides and Proteins - metabolism | HMGB1 Protein - genetics | Antigens, CD - metabolism | HMGB1 Protein - pharmacology | Actin Cytoskeleton - drug effects | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Receptor for Advanced Glycation End Products - genetics | Intracellular Signaling Peptides and Proteins - genetics | Endothelial Cells - physiology | Protein-Serine-Threonine Kinases - metabolism | Actin Cytoskeleton - metabolism | Receptor for Advanced Glycation End Products - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | p38 Mitogen-Activated Protein Kinases - genetics | Recombinant Proteins - genetics | Electric Impedance | Recombinant Proteins - pharmacology | Pulmonary Artery - cytology | Stress Fibers - metabolism | Signal Transduction - drug effects | Endothelial Cells - cytology | Models, Biological | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cytoskeleton - metabolism | HSP27 Heat-Shock Proteins - metabolism | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Gap Junctions - drug effects | Cytoskeleton - drug effects | Endothelial Cells - drug effects | Acute respiratory distress syndrome | Heat shock proteins | Chromosomal proteins | Permeability | Index Medicus | endothelium | acute lung injury
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2012, Volume 7, Issue 4, pp. e36019 - e36019
Yersinia outer protein J (YopJ) is a type III secretion system (T3SS) effector of pathogenic Yersinia (Yersinia pestis, Yersinia enterocolitica and Yersinia... 
INDUCED CELL-DEATH | PROINFLAMMATORY CYTOKINE | LEGIONELLA-PNEUMOPHILA | DENDRITIC CELLS | BACTERIA-FACED MACROPHAGES | CHROMATIN PROTEIN HMGB1 | MULTIDISCIPLINARY SCIENCES | NLRP3 INFLAMMASOME | NF-KAPPA-B | III SECRETION SYSTEM | NALP3 INFLAMMASOME | Caspase 7 - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Caspase 3 - metabolism | Caspase 1 - metabolism | Yersinia - pathogenicity | Interleukin-1beta - metabolism | HMGB1 Protein - metabolism | bcl-2-Associated X Protein - deficiency | Macrophages - microbiology | Yersinia pestis - metabolism | Yersinia Infections - pathology | Yersinia enterocolitica - pathogenicity | Yersinia Infections - microbiology | bcl-2-Associated X Protein - metabolism | Cathepsin B - metabolism | Caspase Inhibitors | Mice, Knockout | Macrophages - metabolism | Yersinia pseudotuberculosis - metabolism | Caspase 1 - deficiency | Yersinia enterocolitica - metabolism | Mice | Enzyme Activation | Yersinia pseudotuberculosis - pathogenicity | bcl-2 Homologous Antagonist-Killer Protein - deficiency | Caspase 8 - metabolism | bcl-2 Homologous Antagonist-Killer Protein - genetics | GTPase-Activating Proteins - metabolism | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Necrosis - pathology | Yersinia Infections - metabolism | Protease Inhibitors - pharmacology | Protein Isoforms - metabolism | Female | Yersinia pestis - pathogenicity | bcl-2-Associated X Protein - genetics | GTPase-Activating Proteins - antagonists & inhibitors | Mice, Inbred C57BL | Bacterial Proteins - genetics | Cells, Cultured | Yersinia - metabolism | Cathepsin B - antagonists & inhibitors | Necrosis - metabolism | Mitochondria - metabolism | Immunity, Innate | Animals | Caspase 1 - genetics | Protein Binding | Bacterial Proteins - metabolism | Protein Isoforms - genetics | Cathepsins | Disease susceptibility | Interleukins | Macrophages | Necrosis | Apoptosis | Salmonella | Bcl-2 protein | Downstream effects | Cytotoxicity | ADP | HMGB1 protein | Caspase-3 | Caspase-1 | Pseudotuberculosis | Signal transduction | Mitochondria | Cell activation | Stress response | Pathogens | Cytokines | Mortality | IL-1β | Metabolism | Gene expression | Caspase-8 | High mobility group proteins | Infectious diseases | Inhibitors | Isoforms | Oxidative stress | Reactive oxygen species | Microscopic analysis | Bax protein | Toxicity | Interleukin | Homology | Infections | Activation | Kinases | Yersinia enterocolitica | Ribose | Cathepsin B | Cell survival | Secretion | Poly(ADP-ribose) polymerase | Caspase | Lymphoma | Polymerase | Lymphocytes B | Cell death | B-cell lymphoma | Index Medicus
Journal Article
Science, ISSN 0036-8075, 3/2009, Volume 323, Issue 5922, pp. 1722 - 1725
Patten recognition receptors, which recognize pathogens or components of injured cells (danger), trigger activation of the innate immune system. Whether and... 
Receptors | Immune response | Cytokines | Hepatocytes | Splenocytes | Liver | Antibodies | Heat shock proteins | Ligands | Reports | Physiological regulation | SYSTEM | ACTIVATION | PROTEIN | AUTOIMMUNITY | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | MOBILITY GROUP BOX-1 | HMGB1 | HEAT-STABLE ANTIGEN | T-CELL GROWTH | ISCHEMIA-REPERFUSION | Liver - pathology | Immunoprecipitation | Receptors, Pattern Recognition - immunology | CD24 Antigen - metabolism | Dendritic Cells - immunology | Humans | HMGB1 Protein - immunology | Receptors, Antigen, B-Cell - metabolism | Necrosis - immunology | Lectins - metabolism | Receptors, Pattern Recognition - metabolism | Liver - immunology | HMGB1 Protein - chemistry | HMGB1 Protein - metabolism | CD24 Antigen - genetics | Protein Structure, Tertiary | Lipopolysaccharides - toxicity | Cytokines - metabolism | Signal Transduction | Acetaminophen - toxicity | Receptors, Cell Surface - metabolism | Mutant Proteins - metabolism | Inflammation - immunology | Immunity, Innate | HSP70 Heat-Shock Proteins - metabolism | Necrosis - chemically induced | Animals | Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism | Transcription Factor RelA - metabolism | Mutant Proteins - chemistry | HSP90 Heat-Shock Proteins - metabolism | Mice | Research | Properties | Cell adhesion molecules | Proteins | Immunology | Cellular biology | Molecular biology | Rodents | Index Medicus
Journal Article
Journal Article