...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular reproduction and development >Mice lacking cyclin-dependent kinase inhibitor p19Ink4d show strain-specific effects on male reproduction.
【24h】

Mice lacking cyclin-dependent kinase inhibitor p19Ink4d show strain-specific effects on male reproduction.

机译：缺乏细胞周期蛋白依赖性激酶抑制剂p19Ink4d的小鼠对雄性生殖表现出菌株特异性作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

p19(Ink4d) is a member of the INK4 family of cyclin-dependent kinase inhibitors, which are important negative regulators of the G1-phase cyclin-dependent kinases CDK4 and CDK6. On a mixed C57BL/6 x 129P2/OlaHsd background, mice deficient for p19(Ink4d) exhibited defects in male reproductive function including testicular atrophy, alteration in serum follicle stimulating hormone, qualitative increase in germ cell apoptosis, and delayed kinetics of meiotic prophase markers (Zindy et al., 2001. Mol Cell Biol 21:3244-3255; Zindy et al., 2000. Mol Cell Biol 20:372-378). In this study, a quantitative assessment of these aspects of reproductive capacity demonstrated relatively mild deficits in p19(Ink4d-/-) males compared to controls. These effects did not dramatically worsen in older males although some seminiferous tubule defects were observed. Following marker-assisted backcrossing into the C57BL/6 background, p19(Ink4d-/-) males did not display defects in testis weights, sperm numbers, serum FSH, germ cellapoptosis, or kinetics of selected meiotic prophase markers. These studies indicate that a reduction in Ink4 family function by the loss of p19(Ink4d) is sufficient to induce mild reproductive defects in male mice with a mixed genetic background, but not in the C57BL/6 genetic background.
机译：p19（Ink4d）是细胞周期蛋白依赖性激酶抑制剂INK4家族的成员，它们是G1期细胞周期蛋白依赖性激酶CDK4和CDK6的重要负调节剂。在混合的C57BL / 6 x 129P2 / OlaHsd背景下，p19（Ink4d）缺陷的小鼠表现出雄性生殖功能缺陷，包括睾丸萎缩，血清卵泡刺激素改变，生殖细胞凋亡的质性增加以及减数分裂前期标志物的动力学延迟（Zindy等，2001.Mol Cell Biol 21：3244-3255; Zindy等，2000.Mol Cell Biol 20：372-378）。在这项研究中，对这些方面的生殖能力进行定量评估表明，与对照组相比，p19（Ink4d-/-）男性的赤字相对较轻。尽管观察到一些曲细精管缺陷，但这些作用在老年男性中并未显着恶化。在标记辅助回交进入C57BL / 6背景后，p19（Ink4d-/-）雄性没有表现出睾丸重量，精子数量，血清FSH，生殖细胞凋亡或所选减数分裂前期标记动力学的缺陷。这些研究表明，p19（Ink4d）的丧失导致Ink4家族功能的降低足以在具有混合遗传背景的雄性小鼠中诱发轻度的生殖缺陷，但在C57BL / 6遗传背景中却不足。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号