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在干扰素合成缺陷的猿猴细胞中外源人β干扰素基因的转录及转录后调控

Transcriptional and posttranscriptional regulation of exogenous human beta interferon gene in simian cells defective in interferon synthesis.

作者信息

Mosca J D, Pitha P M

出版信息

Mol Cell Biol. 1986 Jun;6(6):2279-83. doi: 10.1128/mcb.6.6.2279-2283.1986.

Abstract

We determined that the defect in beta interferon induction in Vero cells is due to the absence of the simian beta interferon (IFN-beta) gene. Nevertheless, the human IFN-beta gene or a hybrid gene, in which the human IFN-beta promoter-regulatory region directs expression of the chloramphenicol acetyltransferase gene (pIFN-CAT), could be induced in transfected Vero cells, and these cells also regulated IFN-beta mRNA (but not pIFN-CAT mRNA) posttranscriptionally. These results indicate that the instability in the human IFN-beta gene is coded for by the coding or 3'-end region of IFN-beta mRNA and that the human IFN-beta gene is regulated in Vero and human cells in an identical manner.

摘要

我们确定,Vero细胞中β干扰素诱导缺陷是由于猿猴β干扰素(IFN-β)基因缺失所致。然而,人IFN-β基因或一种杂合基因(其中人IFN-β启动子调控区指导氯霉素乙酰转移酶基因(pIFN-CAT)的表达)在转染的Vero细胞中可被诱导,并且这些细胞在转录后也调控IFN-β mRNA(但不调控pIFN-CAT mRNA)。这些结果表明,人IFN-β基因的不稳定性由IFN-β mRNA的编码区或3'端区域编码,并且人IFN-β基因在Vero细胞和人细胞中的调控方式相同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a8/367773/84deff60518a/molcellb00090-0436-a.jpg

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