In vitro translational activity of messenger-RNA isolated from mice treated with the interferon inducer, polyriboinosinic acid.polyribocytidylic acid.

In vitro translational activity of messenger-RNA isolated from mice treated with the interferon inducer, polyriboinosinic acid.polyribocytidylic acid.
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从用干扰素诱导剂聚核糖肌苷酸.聚核糖胞苷酸治疗的小鼠中分离出的信使RNA的体外翻译活性。

DOI:
10.1016/0006-2952(90)90201-u
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发表时间:
1990
影响因子:
5.8
通讯作者:
Mannering,GJ
Mannering,GJ
中科院分区:
医学2区
文献类型:
--
作者:
Gooderham,NJ;Mannering,GJ

文献摘要

相似文献

用干扰素和干扰素诱导剂治疗小鼠导致许多肝蛋白下调。在先前的出版物中,证明了这些治疗抑制肝蛋白质合成并增加蛋白质降解,特别是内质网古德勒姆NJ和Mannering GJ,Arch Biochem Biopolymer 250:418-425,1986。在本研究中,研究了聚核糖肌苷酸-聚核糖胞苷酸(poly IC)处理对小鼠肝RNA水平和该RNA在无细胞系统中的翻译的影响。小鼠的Poly IC处理增加了肝脏Poly(A+)RNA水平。在给予poly IC后的不同时间间隔评价分离的poly(A+)RNA的翻译。翻译略有增加,在3-6小时后治疗和抑郁后12-18小时。抗体被用来检查多聚IC治疗对特定多肽的影响,以评估thein体外翻译的酪氨酸转氨酶和白蛋白的mRNA,这些蛋白质的翻译是双相的明显抑郁症。这些研究表明,体内干扰素可能通过增加转录和减少翻译改变肝蛋白水平来调节基因表达。
Treatment of mice with interferon and interferon inducers causes down regulation of a number of hepatic proteins. In a previous publication it was demonstrated that these treatments depress hepatic protein synthesis and increase protein degradation, particularly of the endoplasmic reticulum Gooderham NJ and Mannering GJ,Arch Biochem Biophys250: 418–425, 1986. In the present study the effects of polyriboinosinic acid-polyribocytidylic acid (poly IC) treatment on mouse hepatic RNA levels and the translation of this RNA in a cell-free system were examined. Poly IC treatment of mice increased hepatic poly (A+)RNA levels. The translation of isolated poly(A+)RNA was evaluated at various intervals after the administration of poly IC. Translation was marginally increased at 3–6 hr after treatment and depressed after 12–18 hr. Antibodies were employed to examine the effects of poly IC treatment on specific polypeptides in order to evaluate thein vitrotranslation of mRNAs for tyrosine aminotransferase and albumin; translation of these proteins was biphasic with pronounced depression. These studies indicate thatin vivointerferon may regulate gene expression by altering levels of hepatic proteins via increased transcription and decreased translation.