Control of autoimmune diabetes in NOD mice by GAD expression or suppression in β-cells

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dc.contributor.authorJi Won Yoon-
dc.contributor.authorChang Soon Yoon-
dc.contributor.authorHye Won Lim-
dc.contributor.authorQ Q Huang-
dc.contributor.authorYup Kang-
dc.contributor.authorKwang Ho Pyun-
dc.contributor.authorK Hirasawa-
dc.contributor.authorR S Sherwin-
dc.contributor.authorHee Sook Jun-
dc.date.accessioned2017-04-19T08:55:55Z-
dc.date.available2017-04-19T08:55:55Z-
dc.date.issued1999-
dc.identifier.issn0036-8075-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/4660-
dc.description.abstractGlutamic and decarboxylase (GAD) is a pancreatic β cell autoantigen in humans and nonobese diabetic (NOD) mice. β Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the β cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of β cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, β cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes.-
dc.publisherAmer Assoc Advancement Science-
dc.titleControl of autoimmune diabetes in NOD mice by GAD expression or suppression in β-cells-
dc.title.alternativeControl of autoimmune diabetes in NOD mice by GAD expression or suppression in β-cells-
dc.typeArticle-
dc.citation.titleScience-
dc.citation.number5417-
dc.citation.endPage1187-
dc.citation.startPage1183-
dc.citation.volume284-
dc.contributor.affiliatedAuthorKwang Ho Pyun-
dc.contributor.alternativeName윤지원-
dc.contributor.alternativeName윤창순-
dc.contributor.alternativeName임혜원-
dc.contributor.alternativeNameHuang-
dc.contributor.alternativeName강엽-
dc.contributor.alternativeName변광호-
dc.contributor.alternativeNameHirasawa-
dc.contributor.alternativeNameSherwin-
dc.contributor.alternativeName전희숙-
dc.identifier.bibliographicCitationScience, vol. 284, no. 5417, pp. 1183-1187-
dc.identifier.doi10.1126/science.284.5417.1183-
dc.description.journalClassY-
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