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1. Full Text MCPIP1 Endoribonuclease Activity Negatively Regulates Interleukin-17-Mediated Signaling and Inflammation
by Garg, Abhishek V and Amatya, Nilesh and Chen, Kong and Cruz, J. Agustin and Grover, Prerna and Whibley, Natasha and Conti, Heather R and Hernandez Mir, Gerard and Sirakova, Tatiana and Childs, Erin C and Smithgall, Thomas E and Biswas, Partha S and Kolls, Jay K and McGeachy, Mandy J and Kolattukudy, Pappachan E and Gaffen, Sarah L
Immunity, ISSN 1074-7613, 09/2015, Volume 43, Issue 3, pp. 475 - 487
Interleukin-17 (IL-17) induces pathology in autoimmunity and infections; therefore, constraint of this pathway is an essential component of its regulation. We... 
negative regulation | Regnase-1 | fungal immunity | autoimmunity | signal transduction | IL-17 | Autoimmunity | Signal transduction | Fungal immunity | Negative regulation | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | IL-17 RECEPTOR | TARGET GENES | CANDIDA-ALBICANS | C/EBP-BETA | GENE-EXPRESSION | HOST-DEFENSE | NECROSIS-FACTOR-ALPHA | MESSENGER-RNA STABILITY | T-CELL | IMMUNOLOGY | Candidiasis - genetics | Oncogene Proteins - genetics | Humans | Encephalomyelitis, Autoimmune, Experimental - immunology | Immunoblotting | Male | Receptors, Interleukin-17 - genetics | Ribonucleases - metabolism | Host-Pathogen Interactions - immunology | Inflammation - metabolism | Lipocalins - genetics | Adaptor Proteins, Signal Transducing - immunology | Pneumonia - immunology | Candida albicans - physiology | Encephalomyelitis, Autoimmune, Experimental - genetics | Receptors, Interleukin-17 - metabolism | Interleukin-6 - metabolism | Pneumonia - genetics | Interleukin-6 - genetics | Oncogene Proteins - metabolism | Signal Transduction - genetics | Candida albicans - immunology | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Interleukin-17 - metabolism | Lipocalin-2 | Lipocalins - immunology | Interleukin-6 - immunology | Pneumonia - metabolism | Ribonucleases - genetics | Encephalomyelitis, Autoimmune, Experimental - metabolism | Receptors, Interleukin-17 - immunology | Interleukin-17 - immunology | Acute-Phase Proteins - genetics | Candidiasis - microbiology | Signal Transduction - immunology | HEK293 Cells | Female | Candidiasis - immunology | Nuclear Proteins - genetics | Oncogene Proteins - immunology | Lipocalins - metabolism | Cell Line | Acute-Phase Proteins - metabolism | Mice, Inbred C57BL | Cells, Cultured | Nuclear Proteins - metabolism | Inflammation - immunology | Nuclear Proteins - immunology | Animals | Ribonucleases - immunology | Adaptor Proteins, Signal Transducing - genetics | Inflammation - genetics | Adaptor Proteins, Signal Transducing - metabolism | Acute-Phase Proteins - immunology | Medical colleges | Nucleases | Interleukins | RNA | Cellular signal transduction | Inflammation | Proteins | Cytokines | Rodents | Fibroblasts | Infections | Kinases | Laboratory animals | Gene expression | Experiments
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2. Full Text Identification of Common Transcriptional Regulatory Elements in Interleukin-17 Target Genes
by Fang Shen and Zihua Hu and Jaya Goswami and Sarah L. Gaffen
Journal of Biological Chemistry, ISSN 0021-9258, 08/2006, Volume 281, Issue 34, pp. 24138 - 24148
Interleukin (IL)-17 is the founding member of a novel family of inflammatory cytokines. Although produced by T cells, IL-17 activates genes and signals typical... 
ISCHEMIA-REPERFUSION INJURY | ACTIVATED PROTEIN-KINASE | CXC CHEMOKINE | MESSENGER-RNA | T-CELL INTERLEUKIN-17 | BIOCHEMISTRY & MOLECULAR BIOLOGY | NECROSIS-FACTOR-ALPHA | AIRWAY SMOOTH-MUSCLE | TNF-ALPHA | KAPPA-B-ZETA | NEUTROPHIL RECRUITMENT | Tumor Necrosis Factor-alpha - metabolism | Oncogene Proteins - genetics | Transcriptional Activation - genetics | Humans | Transcriptional Activation - drug effects | Tumor Necrosis Factor-alpha - genetics | Acute-Phase Proteins - genetics | Interleukin-17 - pharmacology | Promoter Regions, Genetic - drug effects | Lipocalins | Transcription, Genetic | CCAAT-Enhancer-Binding Proteins - genetics | Proto-Oncogene Proteins - metabolism | Recombinant Proteins - metabolism | Cell Line | Gene Targeting | Acute-Phase Proteins - metabolism | Oncogene Proteins - metabolism | Interleukin-17 - genetics | Proto-Oncogene Proteins - genetics | Recombinant Proteins - genetics | Signal Transduction - genetics | Binding Sites - genetics | Recombinant Proteins - pharmacology | Drug Synergism | Interleukin-17 - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Animals | NF-kappa B - genetics | Signal Transduction - drug effects | Lipocalin-2 | Protein Binding | Mice
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3. Full Text Dysbiosis and zonulin upregulation alter gut epithelial and vascular barriers in patients with ankylosing spondylitis
by Ciccia, Francesco and Guggino, Giuliana and Rizzo, Aroldo and Alessandro, Riccardo and Luchetti, Michele Maria and Milling, Simon and Saieva, Laura and Cypers, Heleen and Stampone, Tommaso and Di Benedetto, Paola and Gabrielli, Armando and Fasano, Alessio and Elewaut, Dirk and Triolo, Giovanni
Annals of the Rheumatic Diseases, ISSN 0003-4967, 06/2017, Volume 76, Issue 6, pp. 1123 - 1132
BackgroundDysbiosis has been recently demonstrated in patients with ankylosing spondylitis (AS) but its implications in the modulation of intestinal immune... 
Ankylosing Spondylitis | Infections | Inflammation | INTESTINAL INFLAMMATION | RESPONSES | CELLS | INFLAMMATORY-BOWEL-DISEASE | COLITIS | MACROPHAGES | HLA-B27 TRANSGENIC RATS | MICROBIOTA | RHEUMATOLOGY | ARTHRITIS | EXPRESSION | Human Umbilical Vein Endothelial Cells | Ileitis - blood | Up-Regulation | Cholera Toxin - blood | Intestinal Mucosa - metabolism | Junctional Adhesion Molecule A - genetics | Tight Junctions - genetics | Humans | Monocytes - immunology | Dysbiosis - microbiology | Ileum - immunology | RNA, Messenger - metabolism | Antigens, CD - genetics | Interleukin-8 | Case-Control Studies | Spondylitis, Ankylosing - immunology | Dysbiosis - immunology | Lipopolysaccharides - blood | Intestinal Mucosa - immunology | Fatty Acid-Binding Proteins - blood | Cadherins - genetics | Tight Junctions - drug effects | Adherens Junctions - genetics | Caco-2 Cells | Carrier Proteins - blood | Acute Disease | Gene Expression | Rats, Transgenic | Acute-Phase Proteins | Membrane Proteins - genetics | Membrane Glycoproteins - blood | Rats | Intestinal Mucosa - microbiology | Permeability | Carrier Proteins - genetics | Bacteria - isolation & purification | Animals | Endothelium - metabolism | Cholera Toxin - genetics | Ileitis - immunology | Anti-Bacterial Agents - pharmacology | Chronic Disease | Ileum - microbiology | HLA-B27 Antigen - genetics | Proteins | Immune response | Analysis | Research | Ankylosing spondylitis | Cells
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4. Full Text Impaired neutrophil function in 24p3 null mice contributes to enhanced susceptibility to bacterial infections
by Liu, Zhuoming and Petersen, Robert and Devireddy, Laxminarayana
Journal of Immunology, ISSN 0022-1767, 05/2013, Volume 190, Issue 9, pp. 4692 - 4706
Lipocalin 24p3 (24p3) is a neutrophil secondary granule protein. 24p3 is also a siderocalin, which binds several bacterial siderophores. It was therefore... 
LISTERIA-MONOCYTOGENES | IMMUNE-RESPONSE | ACUTE-PHASE PROTEIN | CANDIDA-ALBICANS | LIPOCALIN 24P3 | HOST-DEFENSE | RESISTANCE | MONOCLONAL-ANTIBODY | IRON | DEFICIENT MICE | IMMUNOLOGY | NIH 3T3 Cells | Oncogene Proteins - genetics | Cytoskeletal Proteins - genetics | Cytoskeleton - immunology | Acute-Phase Proteins - genetics | Phagocytosis - genetics | Respiratory Burst - immunology | Bacterial Infections - genetics | Disease Susceptibility - immunology | Bacterial Infections - immunology | Lipocalins - genetics | Cytoskeletal Proteins - metabolism | rho GTP-Binding Proteins - immunology | Chemotaxis - immunology | Neutrophils - metabolism | Oncogene Proteins - immunology | Chemokines - immunology | Lipocalins - metabolism | Cell Line | Acute-Phase Proteins - metabolism | Siderophores - metabolism | rho GTP-Binding Proteins - genetics | Mice, Inbred C57BL | Cytoskeleton - genetics | Neutrophils - immunology | Oncogene Proteins - metabolism | Phagocytosis - immunology | Chemokines - genetics | Chemotaxis - genetics | Mice, Knockout | Animals | Cytoskeletal Proteins - immunology | Lipocalin-2 | Lipocalins - immunology | rho GTP-Binding Proteins - metabolism | Cytoskeleton - metabolism | Chemokines - metabolism | Mice | MicroRNAs - genetics | Respiratory Burst - genetics | Siderophores - immunology | Acute-Phase Proteins - immunology | Bacterial Infections - metabolism | Candida albicans | Listeria monocytogenes | neutrophils | Lipocalin 24p3 | Staphylococcus aureus
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5. Full Text Determinants of Serum Concentrations of Lipopolysaccharide-Binding Protein (LBP) in the Adult Population: The Role of Obesity
by Gonzalez-Quintela, Arturo and Alonso, Manuela and Campos, Joaquin and Vizcaino, Luis and Loidi, Lourdes and Gude, Francisco
PLoS ONE, ISSN 1932-6203, 01/2013, Volume 8, Issue 1, p. e54600
Background and Aim: Assessment of serum concentration of lipopolysaccharide (LPS)-binding protein (LBP) has been suggested as a useful biomarker to indicate... 
INCREASED INTESTINAL PERMEABILITY | THE-159C/T POLYMORPHISM | PLASMA-LEVELS | HIGH-DENSITY | MULTIDISCIPLINARY SCIENCES | GAMMA-GLUTAMYL-TRANSFERASE | PROMOTER REGION | ALCOHOL-CONSUMPTION | POTENTIAL ROLE | BACTERIAL-ENDOTOXIN | INCREASING PROTEIN | Age Factors | Obesity - immunology | Humans | Middle Aged | Male | Acute-Phase Proteins - genetics | Obesity - blood | Obesity - genetics | Inflammation - blood | Metabolic Syndrome - blood | Adult | Female | Metabolic Syndrome - immunology | Carrier Proteins - blood | Genetic Association Studies | Membrane Glycoproteins - blood | Toll-Like Receptor 4 - genetics | Inflammation - immunology | Immunity, Innate | Membrane Glycoproteins - genetics | Carrier Proteins - genetics | Metabolic Syndrome - genetics | Adolescent | Inflammation - genetics | Lipopolysaccharide Receptors - genetics | Polymorphism, Single Nucleotide | Obesity | Blood cholesterol | Liver | Genetic aspects | Research | Mitogens | Genetic polymorphisms | Protein binding | Immunoassay | Demography | Low concentrations | Genes | Body weight | Source studies | Alcohol | Cardiovascular disease | Males | Metabolic syndrome | CD14 antigen | Lipopolysaccharides | Interleukin 6 | Proteins | Demographics | Microorganisms | Rodents | Toll-like receptors | Measurement methods | Population | Bioindicators | Lipoproteins (high density) | Interleukin 8 | Age | Immune system | Consumption | Lipopolysaccharide-binding protein | Immune response | Cytokines | Internal medicine | Abnormalities | Glycoproteins | Inflammation | TLR4 protein | Cholesterol | Serum levels | Lipoproteins | Biomarkers | Sepsis | Adults | Lifestyles | Metabolic disorders | Smoking
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6. Full Text Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2
by El Karoui, Khalil and Viau, Amandine and Dellis, Olivier and Bagattin, Alessia and Nguyen, Clément and Baron, William and Burtin, Martine and Broueilh, Mélanie and Heidet, Laurence and Mollet, Géraldine and Druilhe, Anne and Antignac, Corinne and Knebelmann, Bertrand and Friedlander, Gérard and Bienaimé, Frank and Gallazzini, Morgan and Terzi, Fabiola
Nature Communications, ISSN 2041-1723, 01/2016, Volume 7, Issue 1, pp. 10330 - 10330
In chronic kidney disease (CKD), proteinuria results in severe tubulointerstitial lesions, which ultimately lead to end-stage renal disease. Here we identify... 
RENAL PROXIMAL TUBULE | APOPTOSIS | IN-VITRO | CALCIUM-ENTRY | CANCER CELLS | ER-STRESS | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | DISEASE | TUBULAR EPITHELIAL-CELLS | END-POINTS | Immunohistochemistry | Oncogene Proteins - genetics | WT1 Proteins - metabolism | Male | Intracellular Signaling Peptides and Proteins - metabolism | Acute-Phase Proteins - genetics | Endoplasmic Reticulum Stress - genetics | Lipocalins - genetics | Mice, Mutant Strains | Female | Membrane Proteins - metabolism | Intracellular Signaling Peptides and Proteins - genetics | WT1 Proteins - genetics | Kidney Diseases - metabolism | Lipocalins - metabolism | Unfolded Protein Response - drug effects | Endoplasmic Reticulum Stress - drug effects | Acute-Phase Proteins - metabolism | Membrane Proteins - genetics | Oncogene Proteins - metabolism | Proteinuria - metabolism | Exons - genetics | Albumins - pharmacology | Animals | Lipocalin-2 | Mice | Kidney Diseases - etiology | Proteinuria - complications | Endoplasmic Reticulum Stress - physiology | Index Medicus
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7. Full Text Oxidized phospholipid inhibition of Toll-Like Receptor (TLR) signaling is restricted to TLR2 and TLR4: Roles for CD14, LPS-binding protein, and MD2 as targets for specificity of inhibition
by Erridge, Clett and Kennedy, Simon and Spickett, Corinne M and Webb, David J
Journal of Biological Chemistry, ISSN 0021-9258, 09/2008, Volume 283, Issue 36, pp. 24748 - 24759
The generation of reactive oxygen species is a central feature of inflammation that results in the oxidation of host phospholipids. Oxidized phospholipids,... 
ACTIVATION | ESCHERICHIA-COLI LIPOPOLYSACCHARIDE | INDUCE | BIOCHEMISTRY & MOLECULAR BIOLOGY | LIPID RAFTS | ENDOTHELIAL-CELLS | LOW-DENSITY-LIPOPROTEIN | HEME OXYGENASE-1 | MONOCYTE CHEMOTACTIC PROTEIN-1 | OXIDATION-PRODUCTS | T-LYMPHOCYTES | Phosphatidylcholines - immunology | Reactive Oxygen Species - metabolism | Toll-Like Receptor 2 - genetics | Membrane Glycoproteins - metabolism | Lymphocyte Antigen 96 - metabolism | Humans | Tumor Necrosis Factor-alpha - genetics | Macrophages, Peritoneal - cytology | Flagellin - pharmacology | Lymphocyte Antigen 96 - agonists | Oxidation-Reduction - drug effects | Tumor Necrosis Factor-alpha - immunology | Toll-Like Receptor 4 - agonists | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Carrier Proteins - immunology | Guanosine - analogs & derivatives | Poly I-C - pharmacology | Macrophages, Peritoneal - immunology | Toll-Like Receptor 4 - genetics | Lipopolysaccharide Receptors - immunology | Toll-Like Receptor 4 - immunology | p38 Mitogen-Activated Protein Kinases - immunology | Toll-Like Receptor 2 - metabolism | Toll-Like Receptor 4 - metabolism | Signal Transduction - drug effects | Lipopolysaccharides - pharmacology | Toll-Like Receptor 2 - immunology | I-kappa B Kinase - immunology | Mice | Mice, Inbred BALB C | Macrophages, Peritoneal - metabolism | Oligodeoxyribonucleotides - pharmacology | Immunologic Factors - pharmacology | Lymphocyte Antigen 96 - immunology | Tumor Necrosis Factor-alpha - metabolism | Toll-Like Receptor 2 - agonists | Acute-Phase Proteins - genetics | Lipopolysaccharide Receptors - metabolism | Lymphocyte Antigen 96 - genetics | Carrier Proteins - agonists | I-kappa B Kinase - metabolism | Reactive Oxygen Species - immunology | Female | Membrane Glycoproteins - immunology | Cell Line | Acute-Phase Proteins - metabolism | Phosphatidylcholines - pharmacology | Membrane Glycoproteins - agonists | p38 Mitogen-Activated Protein Kinases - genetics | I-kappa B Kinase - genetics | Membrane Glycoproteins - genetics | Carrier Proteins - genetics | Phosphatidylcholines - genetics | Animals | Carrier Proteins - metabolism | RNA - pharmacology | Guanosine - pharmacology | Lipopolysaccharide Receptors - genetics | Signal Transduction - physiology | Acute-Phase Proteins - agonists | Acute-Phase Proteins - immunology | Lipids and Lipoproteins | Metabolism, Regulation, and Signaling
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8. Full Text Adipocytokines and insulin resistance: the possible role of lipocalin-2, retinol binding protein-4, and adiponectin
by Esteve, Eduardo and Ricart, Wifredo and Fernández-Real, José Manuel
Diabetes care, ISSN 0149-5992, 2009, Volume 32, Issue 11, pp. S362 - 367
Conversely, LCN2 has recently been claimed to display anti-inflammatory effects, so that increased LCN2 levels in obesity and insulin resistance may constitute... 
SERUM RETINOL-BINDING-PROTEIN-4 | OBESITY | ENDOCRINOLOGY & METABOLISM | FAT | SENSITIVITY | CORONARY-HEART-DISEASE | IDENTIFICATION | RECEPTORS | EXPRESSION | NONOBESE SUBJECTS | ADOLESCENT | Lipocalins - metabolism | Proto-Oncogene Proteins - metabolism | Oncogene Proteins - genetics | Glucose Intolerance - genetics | Acute-Phase Proteins - metabolism | Humans | RNA, Messenger - genetics | Oncogene Proteins - metabolism | Proto-Oncogene Proteins - genetics | Acute-Phase Proteins - genetics | Mice, Knockout | Adipose Tissue - metabolism | Animals | Lipocalin-2 | Lipocalins - genetics | Adipokines - genetics | Adiponectin - genetics | Adiponectin - deficiency | Insulin Resistance - genetics | Mice | Retinol-Binding Proteins, Plasma - genetics | Chromosomes, Human, Pair 10 | Cytokines - genetics | Disease Models, Animal | Type 2 diabetes | Colony-stimulating factors (Physiology) | Insulin resistance | Hypoglycemic agents | Chemical properties | Retinoids | Cardiovascular diseases | Peptide hormones | Binding proteins | Macrophages | Protein binding | Proteins | Cardiovascular disease | Diabetes | Insulin | Obesity and Lipids
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9. Full Text The multifaceted roles of neutrophil gelatinase associated lipocalin (NGAL) in inflammation and cancer
by Chakraborty, Subhankar and Kaur, Sukhwinder and Guha, Sushovan and Batra, Surinder K
BBA - Reviews on Cancer, ISSN 0304-419X, 08/2012, Volume 1826, Issue 1, pp. 129 - 169
Neutrophil gelatinase associated lipocalin (NGAL), also known as oncogene 24p3, uterocalin, siderocalin or lipocalin 2, is a 24 kDa secreted glycoprotein... 
NGAL | Lipocalin 2 | 24p3 | Prognosis | Diagnosis | Uterocalin | ACUTE KIDNEY INJURY | URINARY BIOMARKERS | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENE-EXPRESSION PROFILES | INITIATE LIFESAVING TREATMENT | FACTOR-KAPPA-B | ACUTE HEART-FAILURE | BIOPHYSICS | ONCOLOGY | CONTRAST-INDUCED NEPHROPATHY | GROWTH-FACTOR | RENAL REPLACEMENT THERAPY | CRITICALLY-ILL PATIENTS | Lipocalins - metabolism | Neoplasms - metabolism | Proto-Oncogene Proteins - metabolism | Oncogene Proteins - genetics | Acute-Phase Proteins - metabolism | Humans | Oncogene Proteins - metabolism | Proto-Oncogene Proteins - genetics | Acute-Phase Proteins - genetics | Inflammation - metabolism | Animals | Neoplasms - genetics | Lipocalin-2 | Lipocalins - genetics | Inflammation - genetics | Immunohistochemistry | Oxidases | Lung diseases, Obstructive | Endothelial growth factors | Leukemia | HLA histocompatibility antigens | Estrogen | Estradiol | Proteins | Liver cancer | Epidermal growth factor | Physiological aspects | Fibroblast growth factors | Vascular endothelial growth factor | Antigens | Corticosteroids | Bacterial infections | Cytochrome oxidase | Calpain | Inflammation | Crohn's disease | Transforming growth factors | Coronary heart disease | Cytochrome c | Histocompatibility antigens | Thyroid cancer | Chronic kidney failure | Analysis | Pancreatic cancer | Stem cells | Hormones, Sex | Kidney diseases | Cancer
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