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c-myc基因外显子1的截短导致c-myc mRNA稳定性延长。

Truncation of exon 1 from the c-myc gene results in prolonged c-myc mRNa stability.

作者信息

Rabbitts P H, Forster A, Stinson M A, Rabbitts T H

出版信息

EMBO J. 1985 Dec 30;4(13B):3727-33. doi: 10.1002/j.1460-2075.1985.tb04141.x.

DOI:10.1002/j.1460-2075.1985.tb04141.x
PMID:4092694
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC554724/
Abstract

The human c-myc gene consists of three exons transcribed from two distinct promoters and the function of the first, noncoding exon is unknown. In COLO 320 cells, there co-exist normal and truncated (i.e., lacking exon 1) c-myc genes, both of which are transcribed. Studies on the turnover of c-myc mRNA show that the normal mRNA has an in vivo half-life of approximately 30 min which is approximately similar to the turnover time of the mRNA in lymphoblastoid cells. However, the truncated mRNA was found to be substantially more stable. This observation was also made with a Burkitt's lymphoma cell line which has a translocated, truncated c-myc gene. Therefore truncation of the c-myc gene can cause the mRNA to be more stable than the full size product suggesting that this can be a crucial factor in the activation of the c-myc oncogene, by exon 1 loss, in chromosomal translocation. The results also suggest a role for exon 1 in the c-myc mRNA degradative mechanism.

摘要

人类c-myc基因由从两个不同启动子转录而来的三个外显子组成,第一个非编码外显子的功能尚不清楚。在COLO 320细胞中,正常的和截短的(即缺少外显子1)c-myc基因共存,二者均可转录。对c-myc mRNA周转的研究表明,正常mRNA在体内的半衰期约为30分钟,这与淋巴母细胞样细胞中mRNA的周转时间大致相似。然而,发现截短的mRNA稳定性显著更高。在一个具有易位、截短的c-myc基因的伯基特淋巴瘤细胞系中也观察到了这一现象。因此,c-myc基因的截短可导致mRNA比全长产物更稳定,这表明在染色体易位过程中,通过外显子1的缺失,这可能是激活c-myc癌基因的一个关键因素。结果还表明外显子1在c-myc mRNA降解机制中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/40f4d5096d11/emboj00279-0093-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/4be2dbeee2d1/emboj00279-0089-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/f87d6bcc07c5/emboj00279-0090-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/1081c6204824/emboj00279-0091-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/0c023d443b29/emboj00279-0092-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/40f4d5096d11/emboj00279-0093-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/4be2dbeee2d1/emboj00279-0089-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/f87d6bcc07c5/emboj00279-0090-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/1081c6204824/emboj00279-0091-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/0c023d443b29/emboj00279-0092-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/554724/40f4d5096d11/emboj00279-0093-a.jpg

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针对TAR RNA结合蛋白TRBP(一种Dicer辅助因子)的小分子干扰RNA可抑制1型人类免疫缺陷病毒长末端重复序列的表达及病毒产生。
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Proc Natl Acad Sci U S A. 1984 Nov;81(21):6798-802. doi: 10.1073/pnas.81.21.6798.
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