CPEB1协调了具有翻译调节的替代3'-UTR形成
Felice-Alessio Bava1, Carolina Eliscovich, Pedro G Ferreira
1Institute for Research in Biomedicine (IRB Barcelona), Baldiri Reixac 10, 08028 Barcelona, Spain.
Nature
|February 26, 2013
概括
细胞质多基化元素结合蛋白1 (CPEB1) 控制信使RNA 3' 未翻译区域 (3' UTR) 的处理. 这种RNA结合蛋白缩短3' UTRs,影响翻译,细胞增殖和癌症.
科学领域:
- 分子生物学分子生物学
- 在RNA生物学,RNA生物学.
- 癌症生物学 癌症生物学
背景情况:
- 超过一半的哺乳动物基因产生多个信使RNA (mRNA) 异型,具有不同的3'未翻译区域 (3' UTR).
- 这些3' UTR 含有对细胞增殖等过程至关重要的调节序列,并且经常与癌症有关.
- 管理替代3' UTR处理的机制在很大程度上仍未定义.
研究的目的:
- 调查细胞质多化元素结合蛋白1 (CPEB1) 在调节替代3' UTR处理中的作用.
- 阐明CPEB1如何与3' UTR处理协调mRNA翻译.
主要方法:
- 研究了CPEB1的亚细胞局部 (细胞核和细胞质).
- 分析了CPEB1与剪接因子和前mRNAs的相互作用.
- 评估了CPEB1对替代多化和替代拼接的影响.
主要成果:
- CPEB1穿到细胞核,并与剪接因子共同定位.
- CPEB1调解了数百个mRNA 3' UTRs的缩短,影响了细胞质翻译效率.
- 通过抑制U2AF65的招募,CPEB1与前mRNAs的结合影响了替代多基化位点的使用和替代拼接.
- 由CPEB1介导的3' UTR缩短与细胞增殖和瘤发生的增加相关.
结论:
- 在控制替代3'UTR处理方面,CPEB1具有新的功能.
- 通过其双核和细胞质活动,CPEB1将3' UTR处理与mRNA翻译调节相结合.
- 在3' UTR处理中CPEB1的作用对了解细胞增殖和癌症发展有影响.
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