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Lewis X- 和 Lewis Y- 含有糖蛋白在雄性生殖系统中的生物合成和分布。

Biosynthesis and distribution of Lewis X- and Lewis Y-containing glycoproteins in the murine male reproductive system.

机构信息

Shanghai Key Laboratory of Molecular Andrology, State Key Laboratory of Molecular Biology, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, Shanghai, People's Republic of China.

出版信息

Glycobiology. 2011 Feb;21(2):225-34. doi: 10.1093/glycob/cwq152. Epub 2010 Sep 28.

Abstract

Although Lewis X (LeX) and Lewis Y (LeY) antigens were thought to play important roles in fertility, fucosyltransferase (Fut)-deficient (Fut1, Fut2 and Fut4) mice which lack LeX or LeY antigen are still fertile. In the present study, the Fut-deficient and wild-type mice were used to measure the expression of Fut mRNA along the mouse male reproductive tract and determine the role of each Fut in the biosynthesis of LeX/LeY antigens, which are conjugated to glycoproteins in the male reproductive system. LeX/LeY-containing glycoproteins were detected in the epididymis, vas deferens, seminal vesicle and coagulating gland, but not in the testis. We demonstrate that the synthesis of LeY-containing glycoproteins in the epididymis and vas deferens is catalyzed by Fut1 and Fut4. In the seminal vesicle and the coagulating gland, they are mainly synthesized by Fut2 and an α-(1,3)-Fut, but not Fut4. The synthesis of LeX-containing glycoproteins in the middle caput epididymis is catalyzed by Fut4 and by Fut4 and Fut2 in the seminal vesicle. We provide evidence that LeX is synthesized in the coagulating gland by Fut9. We found that the lack of activity by one Fut does not completely inhibit LeX/LeY antigen expression in the male reproductive tract. This redundancy may help to explain why in vivo studies with Fut-deficient mice do not support the presumption that LeX/LeY antigens play important roles in male fertility. We provide details regarding the phenotypes of established Fut-deficient mice and lay the foundation for elucidating the functions of LeX/LeY antigens in other aspects of the male reproductive system.

摘要

虽然 Lewis X (LeX) 和 Lewis Y (LeY) 抗原被认为在生育中发挥重要作用,但缺乏 LeX 或 LeY 抗原的 Fut-缺陷(Fut1、Fut2 和 Fut4)小鼠仍然具有生育能力。在本研究中,使用 Fut 缺陷型和野生型小鼠沿雄性生殖道测量 Fut mRNA 的表达,并确定每个 Fut 在 LeX/LeY 抗原生物合成中的作用,这些抗原与雄性生殖系统中的糖蛋白结合。LeX/LeY 包含的糖蛋白在附睾、输精管、精囊和凝固腺中检测到,但在睾丸中未检测到。我们证明,附睾和输精管中 LeY 包含的糖蛋白的合成由 Fut1 和 Fut4 催化。在精囊和凝固腺中,它们主要由 Fut2 和 α-(1,3)-Fut 合成,但不是 Fut4。中附睾头部 LeX 包含的糖蛋白的合成由 Fut4 和 Fut2 催化。我们提供的证据表明 Fut9 在凝固腺中合成 LeX。我们发现 Fut 缺乏活性并不能完全抑制雄性生殖道中 LeX/LeY 抗原的表达。这种冗余可能有助于解释为什么 Fut 缺陷型小鼠的体内研究不支持 LeX/LeY 抗原在雄性生育力中发挥重要作用的假设。我们提供了关于已建立的 Fut 缺陷型小鼠表型的详细信息,并为阐明 LeX/LeY 抗原在雄性生殖系统其他方面的功能奠定了基础。

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