作者: Emi Ito , Ritsuko Oka , Takeo Ishii , Hiroaki Korekane , Ayako Kurimoto
DOI: 10.1016/J.JPROT.2015.07.011
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摘要: Abstract We previously reported that knockout mice for α1,6-fucosyltransferase ( Fut8 ), which catalyzes the biosynthesis of core-fucose in N -glycans, develop emphysema and heterozygous are more sensitive to cigarette smoke-induced than wild-type mice. Moreover, a lower FUT8 activity was found be associated with faster decline lung function among chronic obstructive pulmonary disease (COPD) patients. These results led us hypothesize core-fucosylation levels glycoprotein could used as biomarker COPD. focused on lung-specific glycoprotein, surfactant protein D (SP-D), plays role immune responses is present distal airways, alveoli, blood circulation. The glycomic analysis herein demonstrate presence an -glycan enriched SP-D from pooled human sera. developed antibody–lectin enzyme immunoassay (EIA) assessing fucosylation (core-fucose α1,3/4 fucose) COPD indicate serum significantly higher patients non-COPD smokers. severity positively Our findings suggest increased development Biological significance It has been proposed concentrations predictive pathogenesis, but distinguishing between healthy individuals establish clear cut-off value difficult because smoking status highly affects circulating levels. Herein, we -glycosylation examined whether or not patterns pathogenesis performed -glycomic show its -glycan. also indeed altered COPD, is, including compared shed new light discovery and/or useful based glycosylation changes diagnosing This article part Special Issue entitled: HUPO 2014.