胰岛素受体和胰岛素样生长因子受体5’UTRs独立于EIF4G1支持翻译起始。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2023-01-01 Epub Date: 2023-10-11 DOI:10.1080/10985549.2023.2255120
Nicholas K Clark, Meghan T Harris, William B Dahl, Zachary Knotts, Michael T Marr
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引用次数: 0

摘要

IRES介导的翻译启动需要与标准帽依赖翻译不同的因素。抑制经典翻译因子EIF4G1的处理对Insr和Igf1r细胞IRESe促进翻译的能力几乎没有影响。两种细胞受体的转录物含有RNA元件,在没有完整EIF4G1的情况下促进翻译起始。细胞IRES机制可能类似于病毒III型IRES,允许它们用有限数量的起始因子促进翻译,允许它们在规范翻译被抑制时在压力条件下工作。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Insulin Receptor and Insulin like Growth Factor Receptor 5' UTRs Support Translation Initiation Independently of EIF4G1.

IRES mediated translation initiation requires a different repertoire of factors than canonical cap-dependent translation. Treatments that inhibit the canonical translation factor EIF4G1 have little or no effect on the ability of the Insr and Igf1r cellular IRESes to promote translation. Transcripts for two cellular receptors contain RNA elements that facilitate translation initiation without intact EIF4G1. Cellular IRES mechanisms may resemble viral type III IRESes allowing them to promote translate with a limited number of initiation factors allowing them to work under stress conditions when canonical translation is repressed.

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CiteScore
7.20
自引率
4.30%
发文量
567
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