...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell cycle >Telomerase enzymatic component hTERT shortens long telomeres in human cells
【24h】

Telomerase enzymatic component hTERT shortens long telomeres in human cells

机译：端粒酶酶成分hTERT缩短人细胞中的长端粒

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

Telomere lengths are tightly regulated within a narrow range in normal human cells. Previous studies have extensively focused on how short telomeres are extended and have demonstrated that telomerase plays a central role in elongating short telomeres. However, much about the molecular mechanisms of regulating excessively long telomeres is unknown. In this report, we demonstrated that the telomerase enzymatic component, hTERT, plays a dual role in the regulation of telomere length. It shortens excessively long telomeres and elongates short telomeres simultaneously in one cell, maintaining the optimal telomere length at each chromosomal end for efficient protection. This novel hTERT-mediated telomere-shortening mechanism not only exists in cancer cells, but also in primary human cells. The hTERT-mediated telomere shortening requires hTERT's enzymatic activity, but the telomerase RNA component, hTR, is not involved in that process. We found that expression of hTERT increases telomeric circular DNA formation, suggesting that telomere homologous recombination is involved in the telomere-shortening process. We further demonstrated that shelterin protein TPP1 interacts with hTERT and recruits hTERT onto the telomeres, suggesting that TPP1 might be involved in regulation of telomere shortening. This study reveals a novel function of hTERT in telomere length regulation and adds a new element to the current molecular model of telomere length maintenance.
机译：在正常人细胞中，端粒的长度在狭窄范围内受到严格调节。先前的研究已广泛关注短端粒的延伸方式，并证明端粒酶在延长短端粒中起着核心作用。然而，调节端粒过长的分子机制尚不清楚。在此报告中，我们证明了端粒酶的酶成分hTERT在端粒长度的调节中起着双重作用。它可在一个细胞中同时缩短过长的端粒并同时延长短的端粒，从而在每个染色体末端保持最佳端粒长度，从而实现有效保护。这种新颖的hTERT介导的端粒缩短机制不仅存在于癌细胞中，而且还存在于原代人细胞中。 hTERT介导的端粒缩短需要hTERT的酶促活性，但端粒酶RNA成分hTR不参与该过程。我们发现hTERT的表达增加端粒环状DNA的形成，这表明端粒同源重组参与端粒缩短过程。我们进一步证明，庇护蛋白TPP1与hTERT相互作用并将hTERT募集到端粒上，这表明TPP1可能参与了端粒缩短的调控。这项研究揭示了hTERT在端粒长度调节中的新功能，并为当前的端粒长度维持分子模型添加了新的元素。

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