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通过转染的酵母基因纠正哺乳动物糖基磷脂酰肌醇锚生物合成中的缺陷。

Correction of a defect in mammalian GPI anchor biosynthesis by a transfected yeast gene.

作者信息

DeGasperi R, Thomas L J, Sugiyama E, Chang H M, Beck P J, Orlean P, Albright C, Waneck G, Sambrook J F, Warren C D

机构信息

Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Massachusetts General Hospital, Boston 02114.

出版信息

Science. 1990 Nov 16;250(4983):988-91. doi: 10.1126/science.1978413.

Abstract

Glycosylphosphatidylinositol (GPI) serves as a membrane anchor for a large number of eukaryotic proteins. A genetic approach was used to investigate the biosynthesis of GPI anchor precursors in mammalian cells. T cell hybridoma mutants that cannot synthesize dolichol-phosphate-mannose (Dol-P-Man) also do not express on their surface GPI-anchored proteins such as Thy-1 and Ly-6A. These mutants cannot form mannose-containing GPI precursors. Transfection with the yeast Dol-P-Man synthase gene rescues the synthesis of both Dol-P-Man and mannose-containing GPI precursors, as well as the surface expression of Thy-1 and Ly-6A, suggesting that Dol-P-Man is the donor of at least one mannose residue in the GPI core.

摘要

糖基磷脂酰肌醇(GPI)作为大量真核生物蛋白质的膜锚定物。采用遗传学方法研究哺乳动物细胞中GPI锚定前体的生物合成。不能合成磷酸多萜醇甘露糖(Dol-P-Man)的T细胞杂交瘤突变体在其表面也不表达GPI锚定蛋白,如Thy-1和Ly-6A。这些突变体不能形成含甘露糖的GPI前体。用酵母Dol-P-Man合酶基因转染可挽救Dol-P-Man和含甘露糖的GPI前体的合成,以及Thy-1和Ly-6A的表面表达,这表明Dol-P-Man是GPI核心中至少一个甘露糖残基的供体。

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