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截断促性腺激素释放激素基因的缺失导致了hpg小鼠的性腺功能减退。

A deletion truncating the gonadotropin-releasing hormone gene is responsible for hypogonadism in the hpg mouse.

作者信息

Mason A J, Hayflick J S, Zoeller R T, Young W S, Phillips H S, Nikolics K, Seeburg P H

出版信息

Science. 1986 Dec 12;234(4782):1366-71. doi: 10.1126/science.3024317.

Abstract

Hereditary hypogonadism in the hypogonadal (hpg) mouse is caused by a deletional mutation of at least 33.5 kilobases encompassing the distal half of the gene for the common biosynthetic precursor of gonadotropin-releasing hormone (GnRH) and GnRH-associated peptide (GAP). The partially deleted gene is transcriptionally active as revealed by in situ hybridization histochemistry of hpg hypothalamic tissue sections, but immunocytochemical analysis failed to show the presence of antigen corresponding to any part of the precursor protein.

摘要

性腺功能减退(hpg)小鼠的遗传性性腺功能减退是由至少33.5千碱基的缺失突变引起的,该突变涵盖促性腺激素释放激素(GnRH)和GnRH相关肽(GAP)共同生物合成前体基因的远端一半。hpg下丘脑组织切片的原位杂交组织化学显示,部分缺失的基因具有转录活性,但免疫细胞化学分析未能显示对应于前体蛋白任何部分的抗原存在。

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