作者: Takashi Miwa , Xiujun Sun , Rieko Ohta , Noriko Okada , Claire L. Harris
DOI: 10.1046/J.1365-2567.2001.01280.X
关键词: Complement receptor 、 Gene 、 Complement system 、 RBBP7 、 Gene expression 、 Decay-accelerating factor 、 Knockout mouse 、 Molecular biology 、 Gene knockout 、 Biology
摘要: Summary Decay-accelerating factor (DAF, CD55) is a glycosylphosphatidylinositol (GPI)-linked membrane inhibitor of complement activation. While human and other mammalian species contain only one DAF gene, two distinct genes, referred to as GPI-DAF transmembrane (TM)-DAF, respectively, have been identified in the mouse. Using several independently generated monoclonal polyclonal antibodies, either with dual or single specificity for TM-DAF gene products, we examined expression genes tissues wild-type strain knockout mouse whose has inactivated. By fluorescence-activated cell sorting (FACS) analysis, found that protein present on erythrocytes lymphocytes but no signal was detectable same cells mice. Both T B splenic macrophages express level higher than lymphocytes. Within population, both CD4+ CD8+ T are positive. detected by immunohistochemistry at high levels spermatids mature sperm. In contrast, sperm stained positive testis, suggesting not expressed spermatids. Examination fetoplacental unit day 7·5 stage revealed maternal decidua surrounding trophoectoderm embryo. No trophoblast embryo proper. These findings suggest although irrelevant blood cells, may different roles germ development and/or function. Because receptor 1-related gene/protein y (Crry) shown be early embryos, complete lack explain observed sensitivity Crry-deficient embryos attack.