<P>Potent antiviral agents hinder virus-infected cell machinery, leading to rescue from viral damage. In this study, we aimed to identify selective intracellular glycosylation inhibitor(s) that do not suppress glycoprotein synthesis. Our results...
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https://www.riss.kr/link?id=A107587208
2010
-
SCOPUS,SCIE
학술저널
115-119(5쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
<P>Potent antiviral agents hinder virus-infected cell machinery, leading to rescue from viral damage. In this study, we aimed to identify selective intracellular glycosylation inhibitor(s) that do not suppress glycoprotein synthesis. Our results...
<P>Potent antiviral agents hinder virus-infected cell machinery, leading to rescue from viral damage. In this study, we aimed to identify selective intracellular glycosylation inhibitor(s) that do not suppress glycoprotein synthesis. Our results showed that nonactin is a potent inhibitor of intracellular glycosylation. First, we examined the effects of nonactin on syncytium formation and cytopathic activity in virus-infected baby hamster kidney cells. Nonactin effectively inhibited syncytium formation in a concentration-dependent manner, and infectious virus production was markedly reduced. However, glycoprotein synthesis was not affected. In the presence of 5 ?g/ml nonactin, we observed the intracellular accumulation of vesicular stomatitis virus-G protein as well as syncytium formation, but no significant effects on Newcastle disease virus-hemagglutinin-neuramidase glycoprotein synthesis. Our results collectively indicate that nonactin potentially inhibits glycosylation by acting as a suppressor of intracellular glycosylation trafficking.</P>
Evaluation of anticancer activity of dehydrocostuslactone in vitro.