Journal of Leukocyte Biology, ISSN 0741-5400, 09/2017, Volume 102, Issue 3, pp. 925 - 939
HIV inhibition of LPS‐induced IL‐27 production in human macrophages affects cIAP‐1‐TRAF‐6, PI3K, and p38 MAPKs. Monocyte‐derived Mϕs (MDMs) from HIV‐infected...
TLR signaling | IL‐27 regulation | HIV infection | IL‐27 expression | IL-27 expression | IL-27 regulation | HUMAN MONOCYTIC CELLS | DENDRITIC CELLS | BINDING PROTEIN BETA | NECROSIS-FACTOR-ALPHA | IMMUNOLOGY | HUMAN-IMMUNODEFICIENCY-VIRUS | CELL BIOLOGY | SINGLE-STRANDED RNA | 2ND CODING EXON | PERIPHERAL-BLOOD MONOCYTES | HEMATOLOGY | NF-KAPPA-B | T-CELLS | Protein Tyrosine Phosphatase, Non-Receptor Type 6 - immunology | Humans | TNF Receptor-Associated Factor 6 - immunology | p38 Mitogen-Activated Protein Kinases - immunology | MAP Kinase Signaling System - immunology | Phosphatidylinositol 3-Kinases - immunology | HIV Infections - immunology | HIV-1 - immunology | MAP Kinase Signaling System - drug effects | Interleukins - immunology | Lipopolysaccharides - pharmacology | Inhibitor of Apoptosis Proteins - immunology | tat Gene Products, Human Immunodeficiency Virus - immunology | Macrophages - immunology | Tumor necrosis factor receptors | Phosphorylation | SHP-1 protein | Peptides | Homology | Intracellular signalling | Infections | Activation | Kinases | Macrophages | Interleukin 27 | Lipopolysaccharides | Signal transduction | Cell activation | Pathways | Human immunodeficiency virus--HIV | Toll-like receptors | Inhibition | Tyrosine | Cytokines | MAP kinase | Interleukin 12 | TLR4 protein | Src protein | 1-Phosphatidylinositol 3-kinase | Tat protein | Monocytes | Intracellular | Protein-tyrosine-phosphatase | Apoptosis
TLR signaling | IL‐27 regulation | HIV infection | IL‐27 expression | IL-27 expression | IL-27 regulation | HUMAN MONOCYTIC CELLS | DENDRITIC CELLS | BINDING PROTEIN BETA | NECROSIS-FACTOR-ALPHA | IMMUNOLOGY | HUMAN-IMMUNODEFICIENCY-VIRUS | CELL BIOLOGY | SINGLE-STRANDED RNA | 2ND CODING EXON | PERIPHERAL-BLOOD MONOCYTES | HEMATOLOGY | NF-KAPPA-B | T-CELLS | Protein Tyrosine Phosphatase, Non-Receptor Type 6 - immunology | Humans | TNF Receptor-Associated Factor 6 - immunology | p38 Mitogen-Activated Protein Kinases - immunology | MAP Kinase Signaling System - immunology | Phosphatidylinositol 3-Kinases - immunology | HIV Infections - immunology | HIV-1 - immunology | MAP Kinase Signaling System - drug effects | Interleukins - immunology | Lipopolysaccharides - pharmacology | Inhibitor of Apoptosis Proteins - immunology | tat Gene Products, Human Immunodeficiency Virus - immunology | Macrophages - immunology | Tumor necrosis factor receptors | Phosphorylation | SHP-1 protein | Peptides | Homology | Intracellular signalling | Infections | Activation | Kinases | Macrophages | Interleukin 27 | Lipopolysaccharides | Signal transduction | Cell activation | Pathways | Human immunodeficiency virus--HIV | Toll-like receptors | Inhibition | Tyrosine | Cytokines | MAP kinase | Interleukin 12 | TLR4 protein | Src protein | 1-Phosphatidylinositol 3-kinase | Tat protein | Monocytes | Intracellular | Protein-tyrosine-phosphatase | Apoptosis
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 01/2004, Volume 279, Issue 4, pp. 2712 - 2718
Pulmonary epithelial cells are continuously exposed to microbial challenges as a result of breathing. It is recognized that immune myeloid cells express...
BACTERIAL LIPOPOLYSACCHARIDE | INTESTINAL EPITHELIUM | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOTOXIN | INVASIVE SHIGELLA-FLEXNERI | GOLGI-APPARATUS | GENE-EXPRESSION | TRANSDUCTION | NF-KAPPA-B | LPS | Cell Line | Toll-Like Receptor 4 | Membrane Glycoproteins - metabolism | Gram-Negative Bacteria | Humans | Receptors, Cell Surface - metabolism | Gram-Negative Bacterial Infections - metabolism | Respiratory Mucosa - ultrastructure | Membrane Glycoproteins - genetics | Cell Compartmentation | Toll-Like Receptors | Signal Transduction - drug effects | Lipopolysaccharides - pharmacology | Respiratory Mucosa - metabolism | Receptors, Cell Surface - genetics | lipopolysaccharides | TLR4 protein
BACTERIAL LIPOPOLYSACCHARIDE | INTESTINAL EPITHELIUM | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOTOXIN | INVASIVE SHIGELLA-FLEXNERI | GOLGI-APPARATUS | GENE-EXPRESSION | TRANSDUCTION | NF-KAPPA-B | LPS | Cell Line | Toll-Like Receptor 4 | Membrane Glycoproteins - metabolism | Gram-Negative Bacteria | Humans | Receptors, Cell Surface - metabolism | Gram-Negative Bacterial Infections - metabolism | Respiratory Mucosa - ultrastructure | Membrane Glycoproteins - genetics | Cell Compartmentation | Toll-Like Receptors | Signal Transduction - drug effects | Lipopolysaccharides - pharmacology | Respiratory Mucosa - metabolism | Receptors, Cell Surface - genetics | lipopolysaccharides | TLR4 protein
Journal Article
Journal of Neurochemistry, ISSN 0022-3042, 03/2016, Volume 136, Issue 5, pp. 958 - 970
Accumulating evidence suggests that activation of microglia plays a key role in the pathogenesis of depression. Activated microglia produce a wide range of...
cytokines | tianeptine | antidepressant drugs | inflammation | microglia | intracellular pathways | Brain | Phosphorylation | Reactive oxygen species | Protein kinase C | Transient ischemic attack | Pathogenesis | Medical services | Disorders | Stimulation | Activation | Mental depression | Kinases | Caspase-3 | Lipopolysaccharides | Degradation | Interleukin 6 | Proteins | Pathways | Antidepressants | Interleukin 1 | Toll-like receptors | Microglial cells | Tumor necrosis factor-TNF | Inhibition | Activation analysis | Immune system | NF-κB protein | Antiinflammatory agents | Cytokines | Extracellular signal-regulated kinase | Caspase | Cultures | Inflammation | TLR4 protein | Nitric-oxide synthase | Microglia | Interleukin 18 | Lymphocytes B | Tumor necrosis factor | Nitric oxide | Tianeptine
cytokines | tianeptine | antidepressant drugs | inflammation | microglia | intracellular pathways | Brain | Phosphorylation | Reactive oxygen species | Protein kinase C | Transient ischemic attack | Pathogenesis | Medical services | Disorders | Stimulation | Activation | Mental depression | Kinases | Caspase-3 | Lipopolysaccharides | Degradation | Interleukin 6 | Proteins | Pathways | Antidepressants | Interleukin 1 | Toll-like receptors | Microglial cells | Tumor necrosis factor-TNF | Inhibition | Activation analysis | Immune system | NF-κB protein | Antiinflammatory agents | Cytokines | Extracellular signal-regulated kinase | Caspase | Cultures | Inflammation | TLR4 protein | Nitric-oxide synthase | Microglia | Interleukin 18 | Lymphocytes B | Tumor necrosis factor | Nitric oxide | Tianeptine
Journal Article
International Journal of Molecular Sciences, ISSN 1661-6596, 07/2018, Volume 19, Issue 7, p. 1965
An increasing body of evidence postulates that microglia are the main mediators of inflammation-related disorders, including depression. Since activated...
M1/M2 microglia activation | Cytokines | NLRP3 inflammasome | Tianeptine | TLR4 intracellular pathways | CANCER-CELLS | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | SCHIZOPHRENIA | KAPPA-B-ALPHA | tianeptine | NEUROTOXICITY | CHEMISTRY, MULTIDISCIPLINARY | NITRIC-OXIDE | cytokines | CENTRAL-NERVOUS-SYSTEM | STRESS | EXPRESSION | HYPOTHALAMUS | Cell Survival - drug effects | Inflammasomes - metabolism | Reactive Oxygen Species - metabolism | Cytokines - metabolism | Microglia - drug effects | NLR Family, Pyrin Domain-Containing 3 Protein - metabolism | Rats | Thiazepines - pharmacology | Rats, Sprague-Dawley | Toll-Like Receptor 4 - metabolism | Animals | Antidepressive Agents, Tricyclic - pharmacology | Lipopolysaccharides - pharmacology | Cell Polarity - drug effects | Cell Death - drug effects | Primary Cell Culture | Nitric Oxide - metabolism | Polarization | Reactive oxygen species | Phosphorylation | CD40 antigen | Insulin-like growth factor I | Interleukin | Activation | Insulin-like growth factors | Mental depression | Kinases | Caspase-1 | Lipopolysaccharides | Interleukin 6 | Interleukin 4 | Antidepressants | Toll-like receptors | Tumor necrosis factor-TNF | Growth factors | Phenotypes | Oligomerization | Extracellular signal-regulated kinase | Caspase | Inflammation | Insulin | Microglia | Interleukin 18 | Beta cells | Molecular modelling | Major histocompatibility complex | Nitric oxide | Interleukin 10 | Histocompatibility | Viability | Monocyte chemoattractant protein 1
M1/M2 microglia activation | Cytokines | NLRP3 inflammasome | Tianeptine | TLR4 intracellular pathways | CANCER-CELLS | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | SCHIZOPHRENIA | KAPPA-B-ALPHA | tianeptine | NEUROTOXICITY | CHEMISTRY, MULTIDISCIPLINARY | NITRIC-OXIDE | cytokines | CENTRAL-NERVOUS-SYSTEM | STRESS | EXPRESSION | HYPOTHALAMUS | Cell Survival - drug effects | Inflammasomes - metabolism | Reactive Oxygen Species - metabolism | Cytokines - metabolism | Microglia - drug effects | NLR Family, Pyrin Domain-Containing 3 Protein - metabolism | Rats | Thiazepines - pharmacology | Rats, Sprague-Dawley | Toll-Like Receptor 4 - metabolism | Animals | Antidepressive Agents, Tricyclic - pharmacology | Lipopolysaccharides - pharmacology | Cell Polarity - drug effects | Cell Death - drug effects | Primary Cell Culture | Nitric Oxide - metabolism | Polarization | Reactive oxygen species | Phosphorylation | CD40 antigen | Insulin-like growth factor I | Interleukin | Activation | Insulin-like growth factors | Mental depression | Kinases | Caspase-1 | Lipopolysaccharides | Interleukin 6 | Interleukin 4 | Antidepressants | Toll-like receptors | Tumor necrosis factor-TNF | Growth factors | Phenotypes | Oligomerization | Extracellular signal-regulated kinase | Caspase | Inflammation | Insulin | Microglia | Interleukin 18 | Beta cells | Molecular modelling | Major histocompatibility complex | Nitric oxide | Interleukin 10 | Histocompatibility | Viability | Monocyte chemoattractant protein 1
Journal Article
Cellular Immunology, ISSN 0008-8749, 09/2013, Volume 285, Issue 1-2, pp. 76 - 83
Recent evidence has shown that dietary phytosterols (PS) possess anti-inflammatory properties both and . Our previous work shows that PS β-Sitosterol (SIT),...
IRAK | Lipid rafts | SOCS | TLR4 | MyD88 | Phytosterols | PHOSPHATASE SHP-1 | CANCER CELLS | CHOLESTEROL | TOLL-LIKE RECEPTOR | IMMUNOLOGY | CELL BIOLOGY | INHIBITION | METABOLISM | GENE-EXPRESSION | OLIGOMERIZATION | Cell Line | Interleukin-1 Receptor-Associated Kinases - metabolism | Toll-Like Receptor 4 - biosynthesis | Interleukin-1 Receptor-Associated Kinases - biosynthesis | Sitosterols - pharmacology | Enzyme Activation - drug effects | Toll-Like Receptor 4 - metabolism | Lipopolysaccharides | Signal Transduction - immunology | Suppressor of Cytokine Signaling 3 Protein | Macrophages - metabolism | Animals | Signal Transduction - drug effects | Membrane Microdomains - drug effects | Mice | Myeloid Differentiation Factor 88 - metabolism | Suppressor of Cytokine Signaling Proteins - biosynthesis | Anticholesteremic Agents - pharmacology | Macrophages - immunology
IRAK | Lipid rafts | SOCS | TLR4 | MyD88 | Phytosterols | PHOSPHATASE SHP-1 | CANCER CELLS | CHOLESTEROL | TOLL-LIKE RECEPTOR | IMMUNOLOGY | CELL BIOLOGY | INHIBITION | METABOLISM | GENE-EXPRESSION | OLIGOMERIZATION | Cell Line | Interleukin-1 Receptor-Associated Kinases - metabolism | Toll-Like Receptor 4 - biosynthesis | Interleukin-1 Receptor-Associated Kinases - biosynthesis | Sitosterols - pharmacology | Enzyme Activation - drug effects | Toll-Like Receptor 4 - metabolism | Lipopolysaccharides | Signal Transduction - immunology | Suppressor of Cytokine Signaling 3 Protein | Macrophages - metabolism | Animals | Signal Transduction - drug effects | Membrane Microdomains - drug effects | Mice | Myeloid Differentiation Factor 88 - metabolism | Suppressor of Cytokine Signaling Proteins - biosynthesis | Anticholesteremic Agents - pharmacology | Macrophages - immunology
Journal Article
Processes, ISSN 2227-9717, 03/2018, Volume 6, Issue 3, p. 21
Due to the intrinsic stochasticity, the signaling dynamics in a clonal population of cells exhibit cell-to-cell variability at the single-cell level, which is...
Lipopolysaccharide | Flow cytometry | Parameter estimation | Sensitivity analysis | NFκB signaling pathway | Systems biology | systems biology | CANCER-CELLS | APOPTOSIS | KINETIC-MODELS | sensitivity analysis | TEMPORAL CONTROL | IDENTIFIABILITY ANALYSIS | RECEPTOR | ENDOCYTOSIS | NF kappa B signaling pathway | INHIBITS PROTEIN-SYNTHESIS | ENGINEERING, CHEMICAL | parameter estimation | flow cytometry | BREFELDIN-A | lipopolysaccharide | TLR4 | Secretion | Intracellular signalling | Tumor necrosis factor-α | Macrophages | Model accuracy | Lipopolysaccharides | Cytometry | Signal transduction | Cell activation | Dynamics | Reagents | Mathematical models | Stochasticity
Lipopolysaccharide | Flow cytometry | Parameter estimation | Sensitivity analysis | NFκB signaling pathway | Systems biology | systems biology | CANCER-CELLS | APOPTOSIS | KINETIC-MODELS | sensitivity analysis | TEMPORAL CONTROL | IDENTIFIABILITY ANALYSIS | RECEPTOR | ENDOCYTOSIS | NF kappa B signaling pathway | INHIBITS PROTEIN-SYNTHESIS | ENGINEERING, CHEMICAL | parameter estimation | flow cytometry | BREFELDIN-A | lipopolysaccharide | TLR4 | Secretion | Intracellular signalling | Tumor necrosis factor-α | Macrophages | Model accuracy | Lipopolysaccharides | Cytometry | Signal transduction | Cell activation | Dynamics | Reagents | Mathematical models | Stochasticity
Journal Article
FOLIA NEUROPATHOLOGICA, ISSN 1641-4640, 2019, Volume 57, Issue 2, pp. 170 - 181
Astragaloside IV (AST-IV) is a major active ingredient of astragalus, with a neuroprotective effect. The current study is aimed to investigate the impact of...
ACTIVATION | neuroinflammatory | ISCHEMIA | MECHANISMS | PATHOLOGY | neurons | NEUROSCIENCES | TLR4 intracellular pathways | microglia polarization | STRATEGIES | astragaloside IV | MICE | INFLAMMATORY CYTOKINES | Neuroprotection | NF-κB protein | Phenotypes | Cell survival | Arginase | Inflammation | TLR4 protein | Tumor necrosis factor-α | Microglia | Lipopolysaccharides | Interleukin 6 | Signal transduction | Molecular modelling | Cell death | Nitric oxide | Interleukin 10 | Toll-like receptors | MyD88 protein | Tumor necrosis factor-TNF | Tumors
ACTIVATION | neuroinflammatory | ISCHEMIA | MECHANISMS | PATHOLOGY | neurons | NEUROSCIENCES | TLR4 intracellular pathways | microglia polarization | STRATEGIES | astragaloside IV | MICE | INFLAMMATORY CYTOKINES | Neuroprotection | NF-κB protein | Phenotypes | Cell survival | Arginase | Inflammation | TLR4 protein | Tumor necrosis factor-α | Microglia | Lipopolysaccharides | Interleukin 6 | Signal transduction | Molecular modelling | Cell death | Nitric oxide | Interleukin 10 | Toll-like receptors | MyD88 protein | Tumor necrosis factor-TNF | Tumors
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2015, Volume 10, Issue 11, p. e0141550
Interleukin (IL)-23 and IL-12 are closely related in structure, and these cytokines regulate both innate and adaptive immunity. However, the precise signaling...
IMMUNE-RESPONSE | ACTIVATION | PROTEIN | MULTIDISCIPLINARY SCIENCES | TOLL-LIKE RECEPTORS | RESISTANCE | INNATE | INFECTION | CYTOKINE | MICE | EXPRESSION | Up-Regulation | Humans | Enzyme Inhibitors - pharmacology | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | MAP Kinase Signaling System | Toxoplasma | Toxoplasmosis - pathology | Toxoplasmosis - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Line, Tumor | Interleukin-23 - biosynthesis | p38 Mitogen-Activated Protein Kinases - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Interleukin-12 - biosynthesis | Care and treatment | Interleukins | Patient outcomes | Physiological aspects | Monoclonal antibodies | Development and progression | Genetic aspects | Research | Health aspects | Networks | Adaptive structures | Phosphorylation | Interleukin | Intracellular signalling | AKT protein | Interleukin 23 | Biology | Infections | Activation | Tachyzoites | Parasites | Kinases | Immunity | Proteins | Signal transduction | Transfection | Pathways | Cascades | Gastroenterology | Toll-like receptors | Inhibition | Pretreatment | Immunoglobulins | Cytokines | Dendritic cells | Secretion | Neutrophils | Extracellular signal-regulated kinase | MAP kinase | Interleukin 12 | JNK protein | siRNA | Adaptive immunity | TLR4 protein | Gene expression | 1-Phosphatidylinositol 3-kinase | Medicine | Monocytes | Hospitals | Inhibitors | TLR2 protein | Wortmannin | Ligands | Intracellular
IMMUNE-RESPONSE | ACTIVATION | PROTEIN | MULTIDISCIPLINARY SCIENCES | TOLL-LIKE RECEPTORS | RESISTANCE | INNATE | INFECTION | CYTOKINE | MICE | EXPRESSION | Up-Regulation | Humans | Enzyme Inhibitors - pharmacology | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | MAP Kinase Signaling System | Toxoplasma | Toxoplasmosis - pathology | Toxoplasmosis - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Line, Tumor | Interleukin-23 - biosynthesis | p38 Mitogen-Activated Protein Kinases - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Interleukin-12 - biosynthesis | Care and treatment | Interleukins | Patient outcomes | Physiological aspects | Monoclonal antibodies | Development and progression | Genetic aspects | Research | Health aspects | Networks | Adaptive structures | Phosphorylation | Interleukin | Intracellular signalling | AKT protein | Interleukin 23 | Biology | Infections | Activation | Tachyzoites | Parasites | Kinases | Immunity | Proteins | Signal transduction | Transfection | Pathways | Cascades | Gastroenterology | Toll-like receptors | Inhibition | Pretreatment | Immunoglobulins | Cytokines | Dendritic cells | Secretion | Neutrophils | Extracellular signal-regulated kinase | MAP kinase | Interleukin 12 | JNK protein | siRNA | Adaptive immunity | TLR4 protein | Gene expression | 1-Phosphatidylinositol 3-kinase | Medicine | Monocytes | Hospitals | Inhibitors | TLR2 protein | Wortmannin | Ligands | Intracellular
Journal Article
PLoS ONE, ISSN 1932-6203, 06/2014, Volume 9, Issue 6, p. e99420
Dendritic cells (DCs) orchestrate host defenses against microorganisms. In infectious diseases due to intracellular bacteria, the inefficiency of the immune...
BRUCELLA | SCRUB TYPHUS | HUMAN MACROPHAGES | DC-SIGN | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | TROPHERYMA-WHIPPLEI | ENDOPLASMIC-RETICULUM | ACTIVATED PROTEIN-KINASES | COXIELLA-BURNETII | ORIENTIA-TSUTSUGAMUSHI | Phosphorylation | Oligonucleotide Array Sequence Analysis | Signal Transduction | Brucella abortus - physiology | Monocytes - cytology | Dendritic Cells - immunology | Humans | Gene Expression Profiling | Coxiella burnetii - physiology | Phenotype | Animals | Interferon-beta - metabolism | Intracellular Space - microbiology | Transcription, Genetic | Cell Differentiation | Mice, Inbred BALB C | p38 Mitogen-Activated Protein Kinases - metabolism | Bacteria | Interferon | Dendritic cells | Biological response modifiers | Analysis | Scrub typhus | Transcription | Genes | Infections | Activation | Kinases | Cytosol | Typhus | Defects | Proteins | Microorganisms | Endocytosis | Immunology | Listeria | Compartments | Toll-like receptors | Trends | Stat1 protein | Immune system | Pathogens | Antigen presentation | Immune response | Bacterial infections | Maturation | TLR4 protein | Gene expression | Fever | TLR3 protein | Monocytes | Infectious diseases | Tuberculosis | DNA microarrays | Q fever | Biomarkers | Brucellosis | Intracellular
BRUCELLA | SCRUB TYPHUS | HUMAN MACROPHAGES | DC-SIGN | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | TROPHERYMA-WHIPPLEI | ENDOPLASMIC-RETICULUM | ACTIVATED PROTEIN-KINASES | COXIELLA-BURNETII | ORIENTIA-TSUTSUGAMUSHI | Phosphorylation | Oligonucleotide Array Sequence Analysis | Signal Transduction | Brucella abortus - physiology | Monocytes - cytology | Dendritic Cells - immunology | Humans | Gene Expression Profiling | Coxiella burnetii - physiology | Phenotype | Animals | Interferon-beta - metabolism | Intracellular Space - microbiology | Transcription, Genetic | Cell Differentiation | Mice, Inbred BALB C | p38 Mitogen-Activated Protein Kinases - metabolism | Bacteria | Interferon | Dendritic cells | Biological response modifiers | Analysis | Scrub typhus | Transcription | Genes | Infections | Activation | Kinases | Cytosol | Typhus | Defects | Proteins | Microorganisms | Endocytosis | Immunology | Listeria | Compartments | Toll-like receptors | Trends | Stat1 protein | Immune system | Pathogens | Antigen presentation | Immune response | Bacterial infections | Maturation | TLR4 protein | Gene expression | Fever | TLR3 protein | Monocytes | Infectious diseases | Tuberculosis | DNA microarrays | Q fever | Biomarkers | Brucellosis | Intracellular
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2013, Volume 8, Issue 5, p. e64373
Background: The migration of hepatic stellate cells (HSCs) is essential to the hepatic fibrotic response, and recently High-mobility group box 1 (HMGB1) has...
APOPTOSIS | PROTEIN | RAT | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | LIVER FIBROSIS | KAPPA-B | HMGB1 | RECEPTOR 4 | EXPRESSION | GLYCATION END-PRODUCTS | Cell Survival - drug effects | Apoptosis - drug effects | Humans | NF-kappa B - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Hepatic Stellate Cells - cytology | Toll-Like Receptor 4 - metabolism | Blotting, Western | Cell Movement - drug effects | HMGB1 Protein - pharmacology | Signal Transduction - drug effects | Cell Proliferation - drug effects | Tumor Cells, Cultured | Proto-Oncogene Proteins c-akt - metabolism | Hepatic Stellate Cells - drug effects | Viral antibodies | Chromosomal proteins | Liver diseases | Collagen | Analysis | Liver | Antibodies | Enzyme-linked immunosorbent assay | Cell proliferation | Phosphorylation | Motility | Mobility | Intracellular signalling | AKT protein | Smooth muscle | Kinases | HMGB1 protein | Cell adhesion & migration | Proteins | Signal transduction | Cell growth | Pathways | Rodents | Gastroenterology | Toll-like receptors | Fibroblasts | Extracellular matrix | Inhibition | Recombinant | Stellate cells | NF-κB protein | Cytokines | JNK protein | TLR4 protein | 1-Phosphatidylinositol 3-kinase | Inhibitors | Neutralizing | Fibrosis | Hypoxia | Intracellular | Cell migration
APOPTOSIS | PROTEIN | RAT | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | LIVER FIBROSIS | KAPPA-B | HMGB1 | RECEPTOR 4 | EXPRESSION | GLYCATION END-PRODUCTS | Cell Survival - drug effects | Apoptosis - drug effects | Humans | NF-kappa B - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Hepatic Stellate Cells - cytology | Toll-Like Receptor 4 - metabolism | Blotting, Western | Cell Movement - drug effects | HMGB1 Protein - pharmacology | Signal Transduction - drug effects | Cell Proliferation - drug effects | Tumor Cells, Cultured | Proto-Oncogene Proteins c-akt - metabolism | Hepatic Stellate Cells - drug effects | Viral antibodies | Chromosomal proteins | Liver diseases | Collagen | Analysis | Liver | Antibodies | Enzyme-linked immunosorbent assay | Cell proliferation | Phosphorylation | Motility | Mobility | Intracellular signalling | AKT protein | Smooth muscle | Kinases | HMGB1 protein | Cell adhesion & migration | Proteins | Signal transduction | Cell growth | Pathways | Rodents | Gastroenterology | Toll-like receptors | Fibroblasts | Extracellular matrix | Inhibition | Recombinant | Stellate cells | NF-κB protein | Cytokines | JNK protein | TLR4 protein | 1-Phosphatidylinositol 3-kinase | Inhibitors | Neutralizing | Fibrosis | Hypoxia | Intracellular | Cell migration
Journal Article
Cellular Microbiology, ISSN 1462-5814, 12/2019, Volume 21, Issue 12, pp. e13095 - n/a
It has been long recognised that activation of toll‐like receptors (TLRs) induces autophagy to restrict intracellular bacterial growth. However, the mechanisms...
AMP‐activated protein kinase | mTOR | toll‐like receptors | ULK1 | autophagy | Salmonella Typhimurium | TARGET | toll-like receptors | PHOSPHORYLATION | MICROBIOLOGY | AMP-activated protein kinase | CELL BIOLOGY | INVASION | EPITHELIAL-CELLS | TAK1 | HOST-DEFENSE | AMPK | INFECTION | TOR protein | Phosphates | Salmonella | Phosphorylation | Gastroenteritis | Food contamination | Flagellin | Intracellular signalling | Activation | Kinases | Macrophages | Autophagy | Lipopolysaccharides | Signal transduction | Receptors | Cell activation | Xenografts | Bone marrow | Toll-like receptors | Bacteria | CpG islands | TLR5 protein | AMP | TAK1 protein | TLR4 protein | TLR9 protein | Signaling | Protein kinase | Food poisoning | Intracellular | Phagocytosis | Index Medicus
AMP‐activated protein kinase | mTOR | toll‐like receptors | ULK1 | autophagy | Salmonella Typhimurium | TARGET | toll-like receptors | PHOSPHORYLATION | MICROBIOLOGY | AMP-activated protein kinase | CELL BIOLOGY | INVASION | EPITHELIAL-CELLS | TAK1 | HOST-DEFENSE | AMPK | INFECTION | TOR protein | Phosphates | Salmonella | Phosphorylation | Gastroenteritis | Food contamination | Flagellin | Intracellular signalling | Activation | Kinases | Macrophages | Autophagy | Lipopolysaccharides | Signal transduction | Receptors | Cell activation | Xenografts | Bone marrow | Toll-like receptors | Bacteria | CpG islands | TLR5 protein | AMP | TAK1 protein | TLR4 protein | TLR9 protein | Signaling | Protein kinase | Food poisoning | Intracellular | Phagocytosis | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2012, Volume 7, Issue 2, p. e32268
The mammalian tachykinins, substance P (SP) and hemokinin-1 (HK-1), are widely distributed throughout the nervous system and/or peripheral organs, and function...
SUPRASPINAL LEVEL | CELLS | PAIN | MESSENGER-RNA | KINASE | BIOLOGY | RAT/MOUSE HEMOKININ-1 | NK1 RECEPTOR | MICE | MAMMALIAN TACHYKININ PEPTIDE | SUBSTANCE-P | Microglia - metabolism | Up-Regulation | Signal Transduction | Tachykinins - metabolism | Gene Expression Regulation | Neurotransmitter Agents - metabolism | Lipopolysaccharides - metabolism | Rats | NF-kappa B - metabolism | RNA, Messenger - metabolism | Rats, Sprague-Dawley | Tachykinins - biosynthesis | Animals | Immune System | Substance P - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Brain | Tachykinin receptors | Peptides | Laboratories | Central nervous system | Intracellular signalling | Nervous system | Neuropeptides | Activation | Kinases | Neuromodulation | Modulators | Medical schools | Proteins | Signal transduction | Pathways | Rodents | Toll-like receptors | Trends | Immune system | NF-κB protein | Substance P | Organs | MAP kinase | Pharmacology | Inflammation | TLR4 protein | Gene expression | Microglia | Neurotransmitters | Brain-derived neurotrophic factor | Protein kinase | Tachykinin
SUPRASPINAL LEVEL | CELLS | PAIN | MESSENGER-RNA | KINASE | BIOLOGY | RAT/MOUSE HEMOKININ-1 | NK1 RECEPTOR | MICE | MAMMALIAN TACHYKININ PEPTIDE | SUBSTANCE-P | Microglia - metabolism | Up-Regulation | Signal Transduction | Tachykinins - metabolism | Gene Expression Regulation | Neurotransmitter Agents - metabolism | Lipopolysaccharides - metabolism | Rats | NF-kappa B - metabolism | RNA, Messenger - metabolism | Rats, Sprague-Dawley | Tachykinins - biosynthesis | Animals | Immune System | Substance P - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Brain | Tachykinin receptors | Peptides | Laboratories | Central nervous system | Intracellular signalling | Nervous system | Neuropeptides | Activation | Kinases | Neuromodulation | Modulators | Medical schools | Proteins | Signal transduction | Pathways | Rodents | Toll-like receptors | Trends | Immune system | NF-κB protein | Substance P | Organs | MAP kinase | Pharmacology | Inflammation | TLR4 protein | Gene expression | Microglia | Neurotransmitters | Brain-derived neurotrophic factor | Protein kinase | Tachykinin
Journal Article