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一种富含A+U元件的RNA结合因子在体外调节c-myc mRNA的稳定性。

An A + U-rich element RNA-binding factor regulates c-myc mRNA stability in vitro.

作者信息

Brewer G

机构信息

Department of Microbiology and Immunology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27103.

出版信息

Mol Cell Biol. 1991 May;11(5):2460-6. doi: 10.1128/mcb.11.5.2460-2466.1991.

DOI:10.1128/mcb.11.5.2460-2466.1991
PMID:1901943
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC360010/
Abstract

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.

摘要

某些原癌基因、细胞因子和转录因子的瞬时表达是细胞对生长因子、12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯、抗原刺激或炎症的一种反应。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'非翻译区中富含A + U的元件作为一种识别信号，靶向这些mRNA进行快速降解。我报告了一种胞质因子的鉴定，该因子既能与原癌基因c - myc富含A + U的元件结合，又能在一个无细胞mRNA降解系统中特异性地使c - myc mRNA不稳定，该系统可重构细胞中发现的mRNA降解过程。用蛋白酶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。这些发现应有助于理解细胞如何选择性地靶向mRNA进行快速周转。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b5/360010/2cd0cd3cb4b6/molcellb00139-0140-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b5/360010/dac93970cae0/molcellb00139-0138-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b5/360010/530f3f4d59bd/molcellb00139-0139-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b5/360010/e79941feab5f/molcellb00139-0140-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b5/360010/2cd0cd3cb4b6/molcellb00139-0140-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b5/360010/dac93970cae0/molcellb00139-0138-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b5/360010/530f3f4d59bd/molcellb00139-0139-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b5/360010/e79941feab5f/molcellb00139-0140-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b5/360010/2cd0cd3cb4b6/molcellb00139-0140-b.jpg

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