S100A8/A9: a mediator of severe asthma pathogenesis and morbidity?
about
Airway symptoms and biological markers in nasal lavage fluid in subjects exposed to metalworking fluidsHouse Dust Mite Allergen Regulates Constitutive Apoptosis of Normal and Asthmatic Neutrophils via Toll-Like Receptor 4Diesel particulate matter induces receptor for advanced glycation end-products (RAGE) expression in pulmonary epithelial cells, and RAGE signaling influences NF-κB-mediated inflammationUpregulation of calprotectin in mild IgE-mediated ovalbumin hypersensitivity.Presence of S100A9-positive inflammatory cells in cancer tissues correlates with an early stage cancer and a better prognosis in patients with gastric cancer.Transgenic expression of human S100A12 induces structural airway abnormalities and limited lung inflammation in a mouse model of allergic inflammationDAMP molecule S100A9 acts as a molecular pattern to enhance inflammation during influenza A virus infection: role of DDX21-TRIF-TLR4-MyD88 pathway.Epithelial regulation of mesenchymal tissue behavior.Expression of RAGE and HMGB1 in thymic epithelial tumors, thymic hyperplasia and regular thymic morphology.Increased heat shock protein 70 levels in induced sputum and plasma correlate with severity of asthma patients.Human eosinophils express RAGE, produce RAGE ligands, exhibit PKC-delta phosphorylation and enhanced viability in response to the RAGE ligand, S100BPulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cellsProteomic analysis reveals the deregulation of inflammation-related proteins in acupuncture-treated rats with asthma onsetRegulation of TLR3 Activation by S100A9.Different faces of hepatocellular carcinoma as a health threat in 21st centuryDecreased S100A9 Expression Promoted Rat Airway Smooth Muscle Cell Proliferation by Stimulating ROS Generation and Inhibiting p38 MAPK.Joining S100 proteins and migration: for better or for worse, in sickness and in health.Transition from identity to bioactivity-guided proteomics for biomarker discovery with focus on the PF2D platform.The TLR4-TRIF pathway can protect against the development of experimental allergic asthma.High-mobility group box 1 promotes extracellular matrix synthesis and wound repair in human bronchial epithelial cells.S100A8, S100A9 and S100A12 activate airway epithelial cells to produce MUC5AC via extracellular signal-regulated kinase and nuclear factor-κB pathways.All the "RAGE" in lung disease: The receptor for advanced glycation endproducts (RAGE) is a major mediator of pulmonary inflammatory responses.A review on symptoms, treatments protocols, and proteomic profile in sulfur mustard-exposed victims.S100A12 and the Airway Smooth Muscle: Beyond Inflammation and Constriction.The receptor for advanced glycation end products is a central mediator of asthma pathogenesis.T-helper 2 cytokine-induced heat shock protein 70 secretion and its potential association with allergic rhinitis.Embryonic overexpression of receptors for advanced glycation end-products by alveolar epithelium induces an imbalance between proliferation and apoptosis.
P2860
Q28393528-21654AD9-07DD-427D-B09A-65FAB5F098CBQ28547246-45E5978B-0AE1-4617-BDBD-407250E87C8EQ28741837-D3AC2A47-23DA-4BE7-B646-215078D26AA2Q33913941-DD1D498B-D157-480E-B24D-0CB5A9CC9CFFQ34354001-FD69E803-3BEF-4D57-BA8A-8C29A5144E84Q34977648-02E74FAF-1D0F-43B9-8EAB-B1C1D5E56536Q35082211-43732CC6-A9A1-456F-A4F5-8D89C61FC43EQ35107649-3E28FB0C-4259-4E99-BD20-58DB5A3A7EF0Q35140467-FD89E48C-471A-41A5-BB17-BA9BAA441B37Q35562247-F933C3D7-689D-49FC-9DA0-D64976EB8857Q35579991-A01DBBB1-F342-422B-8759-5741C6896ADCQ36037610-3EE26A40-2B1C-4B9D-B518-BF6DDC5D1277Q36471128-639D9BE2-F1FD-4DE5-BCC1-BAF325CBAAD7Q36561303-E4C12A54-FED3-4FAC-AA64-EED9756EBE2BQ36783264-9E4867C8-3582-4848-9397-01CC1FB75AE4Q37512694-8DE9F799-FA2B-4C8F-9024-6F45A8D085E7Q38118075-3C91835C-2DCF-4BF3-8100-3AE28B74CD09Q38552059-6159AE2B-391A-4335-A43D-B4E8FECF2D3BQ38787350-65FD30AE-EFC3-4C3B-BF15-1B5FC094A3EDQ38830593-359B1216-001A-4E33-BD7C-29BE19B22D4DQ38979965-2469C17B-A14E-45C5-B414-84EF78BDADB9Q39246681-43B5D19C-AD4E-4500-80A4-9411120E321EQ39402372-2B1917B2-767A-4C6F-9172-BC5AFB16D813Q40659883-8BB6F728-884B-447C-ABE6-0869C14A943CQ42044686-6514BFA8-3015-479D-A79A-D488A237C84AQ50971659-59C00D3C-399B-43FF-BCA7-FCBE43C05649Q51813931-605E1F6B-6AE8-470A-B73E-BE0A78964478
P2860
S100A8/A9: a mediator of severe asthma pathogenesis and morbidity?
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on October 2009
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
S100A8/A9: a mediator of severe asthma pathogenesis and morbidity?
@en
S100A8/A9: a mediator of severe asthma pathogenesis and morbidity?
@nl
type
label
S100A8/A9: a mediator of severe asthma pathogenesis and morbidity?
@en
S100A8/A9: a mediator of severe asthma pathogenesis and morbidity?
@nl
prefLabel
S100A8/A9: a mediator of severe asthma pathogenesis and morbidity?
@en
S100A8/A9: a mediator of severe asthma pathogenesis and morbidity?
@nl
P2860
P356
P1476
S100A8/A9: a mediator of severe asthma pathogenesis and morbidity?
@en
P2093
Saeid Ghavami
P2860
P304
P356
10.1139/Y09-054
P577
2009-10-01T00:00:00Z