AN A+U-RICH ELEMENT RNA-BINDING FACTOR REGULATES C-MYC MESSENGER-RNA STABILITY INVITRO
AN A+U-RICH ELEMENT RNA-BINDING FACTOR REGULATES C-MYC MESSENGER-RNA STABILITY INVITRO
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DOI：
10.1128/mcb.11.5.2460
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发表时间：
1991-05-01
影响因子：
5.3
通讯作者：
BREWER, G
中科院分区：
文献类型：
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作者：
BREWER, G
一些原癌基因、细胞因子和转录因子的短暂表达是细胞对生长因子、12- o-十四烷酰基磷酸-13-乙酸、抗原刺激或炎症的反应。这些基因的表达部分是由其mrna的快速周转介导的。这些mrna的3'非翻译区富含A + u的元素作为一种识别信号，靶向mrna进行快速降解。我报告了一种细胞质因子的鉴定，该因子既与原癌基因c-myc a + u富元素结合，又在无细胞mRNA衰变系统中特异性地破坏c-myc mRNA的稳定性，该系统重建了细胞中发现的mRNA衰变过程。蛋白酶K处理该因子可消除其c-myc mRNA降解活性，而不影响其rna结合能力。因此，RNA底物结合和降解似乎是可分离的功能。这些发现有助于理解细胞如何选择性地靶向mrna以实现快速周转。
Transient expression of some proto-oncogenes, cytokines, and transcription factors occurs as a cellular response to growth factors, 12-O-tetradecanoylphorbol-13-acetate, antigen stimulation, or inflammation. Expression of these genes is mediated in part by the rapid turnover of their mRNAs. A + U-rich elements in the 3' untranslated regions of these mRNAs serve as one recognition signal targeting the mRNAs for rapid degradation. I report the identification of a cytosolic factor that both binds to the proto-oncogene c-myc A + U-rich element and specifically destabilizes c-myc mRNA in a cell-free mRNA decay system which reconstitutes mRNA decay processes found in cells. Proteinase K treatment of the factor abolishes its c-myc mRNA degradation activity without affecting its RNA-binding capacity. Thus, RNA substrate binding and degradation appear to be separable functions. These findings should aid in understanding how the cell selectively targets mRNAs for rapid turnover.