Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is widely known that the cockroach is an inhalant allergen in atopic asthma and allergic rhinitis. Even though Bla g I and Bla g II are considered as the major allergens, several relatively high-molecular weight (MW) cockroach allergens have also been recently identified by IgE-immunoblot in western countries. However, the environmental control and diagnostic tests mainly focussed on Bla g I and Bla g II. Furthermore there is no data about major IgE-binding cockroach antigens in Korea. We performed this study to identify the major German cockroach allergens in Korean atopic children. By the results of allergy skin tests, 14 children with atopic asthma (9 were cockroach-sensitive and 5 were cockroach-nonsensitive atopics) were enrolled in this study. We conducted IgE immunoblot and autoradiographic analysis using Yonsei-extract of German cockroach antigen produced in our laboratory, individual sera from 9 cockroach-sensitive children, and the pooled sera of 5 house-dust-mites-only-sensitive children. We performed an allergic skin test to cockroach mix, and a radioallergosorbent test (RAST) using German cockroach crude extract on all subjects. German cockroach-specific IgE was detected in 6 out of 9 subjects by RAST. We identified at least 15 IgE-binding protein bands, and among them, the components of MWs of 76, 64, 50, 38, and < 14 kilodaltons (kDa) were the major German cockroach allergens in study subjects. Therefore, Bla g I (25-30 kDa) and Bla g II (36 kDa) could not be the absolute indicators of German cockroach sensitization and parameters of environmental control.
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PMID:IgE binding patterns to German cockroach whole body extract in Korean atopic asthmatic children. 982 89

Peroxisome proliferator activated receptor gamma (PPAR-gamma) agonists are involved in the regulation of inflammatory responses and recent studies suggest that PPAR-gamma ligands may have potential for the treatment of allergic airway disease. This study investigated the effect of the PPAR-gamma agonist, rosiglitazone, on nasal mucous allergic inflammation and galectin-3 gene expression in a murine model of allergic rhinitis (AR mice). Rosiglitazone resulted in a statistically significant attenuation of the increased numbers of inflammatory cells and Th2 cytokine levels in nasal cavity lavage fluid of AR mice. Furthermore, the expression of galectin-3 in the nasal mucosa of AR mice was statistically significantly increased. Overexpression of galectin-3 was markedly suppressed by rosiglitazone treatment. These data suggest that the PPAR-gamma agonist, rosiglitazone, may have potential in the development of therapies for allergic rhinitis.
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PMID:Rosiglitazone attenuates allergic inflammation and inhibits expression of galectin-3 in a mouse model of allergic rhinitis. 1865 80