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上游开放阅读框对CCAAT/增强子结合蛋白α和β翻译的抑制作用。

Inhibition of CCAAT/enhancer-binding protein alpha and beta translation by upstream open reading frames.

作者信息

Lincoln A J, Monczak Y, Williams S C, Johnson P F

机构信息

Advanced BioScience Laboratories-Basic Research Program, NCI-Frederick Cancer Research and Development Center, National Institutes of Health, Frederick, Maryland 21702-1201, USA.

出版信息

J Biol Chem. 1998 Apr 17;273(16):9552-60. doi: 10.1074/jbc.273.16.9552.

Abstract

CCAAT/enhancer-binding protein (C/EBP) alpha is a bZIP transcription factor whose expression is restricted to specific cell types. Analysis of C/EBPalpha mRNA and protein levels in various mammalian cells indicates that expression of this gene is controlled both transcriptionally and post-transcriptionally. We report here that C/EBPalpha translation is repressed in several cell lines by an evolutionarily conserved upstream open reading frame (uORF), which acts in cis to inhibit C/EBPalpha translation. Mutations that disrupt the uORF completely abolished translational repression of C/EBPalpha. The related c/ebpbeta gene also contains an uORF that suppresses translation. The length of the spacer sequence between the uORF terminator and the ORF initiator codon (7 bases in all c/ebpalpha genes and 4 bases in c/ebpbeta homologs) is precisely conserved. The effects of insertions, deletions, and base substitutions in the C/EBPalpha spacer showed that both the length and nucleotide sequence of the spacer are important for efficient translational repression. Our data indicate that the uORFs regulate translation of full-length C/EBPalpha and C/EBPbeta and do not play a role in generating truncated forms of these proteins, as has been suggested by start site multiplicity models.

摘要

CCAAT/增强子结合蛋白(C/EBP)α是一种bZIP转录因子,其表达仅限于特定细胞类型。对各种哺乳动物细胞中C/EBPα mRNA和蛋白质水平的分析表明,该基因的表达在转录和转录后水平均受到调控。我们在此报告,C/EBPα的翻译在几种细胞系中受到一个进化上保守的上游开放阅读框(uORF)的抑制,该uORF顺式作用以抑制C/EBPα的翻译。破坏uORF的突变完全消除了C/EBPα的翻译抑制。相关的c/ebpβ基因也含有一个抑制翻译的uORF。uORF终止密码子与开放阅读框起始密码子之间的间隔序列长度(所有c/ebpα基因中为7个碱基,c/ebpβ同源物中为4个碱基)精确保守。C/EBPα间隔区的插入、缺失和碱基替换的影响表明,间隔区的长度和核苷酸序列对于有效的翻译抑制都很重要。我们的数据表明,uORF调节全长C/EBPα和C/EBPβ的翻译,并且如起始位点多样性模型所暗示的那样,在产生这些蛋白质的截短形式中不起作用。

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