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首页> 外文期刊>Molecular and Cellular Biology >Induction of a rapidly responsive hepatic gene product by thyroid hormone requires ongoing protein synthesis.
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Induction of a rapidly responsive hepatic gene product by thyroid hormone requires ongoing protein synthesis.

机译：甲状腺激素诱导快速反应的肝基因产物需要持续的蛋白质合成。

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The regulation of a gene, designated spot 14, which is rapidly induced in rat liver in response to 3,5,3'-triiodo-L-thyronine (T3) was studied as a model for exploring the molecular basis of thyroid hormone action. The time course of induction of the nuclear precursor to spot 14 mRNA after intramuscular injection of T3 displayed a very short lag period of between 10 and 20 min. The rapidity of this effect suggests that the induction in gene expression occurs as a primary response to the hormone-receptor interaction. The protein synthesis inhibitor cycloheximide injected 15 min before T3 completely blocked the accumulation of nuclear precursor RNA 30 min after T3 treatment. Emetine, an inhibitor of protein synthesis which acts by a different mechanism than cycloheximide, also blocked the induction of the spot 14 nuclear precursor RNA. The increased rate of spot 14 gene transcription observed after T3 treatment, as measured by nuclear run-on assay, was similarly completely abolished in the presence of cycloheximide. In addition, ongoing protein synthesis was required for maintaining spot 14 nuclear precursor RNA at induced levels in animals previously treated with T3. On the other hand, cycloheximide had no effect on T3 uptake or binding to the nuclear receptor during the 45-min time frame studied. The paradox of the rapid kinetics of induction and the requirement of ongoing protein synthesis may be explained by a protein with an extremely short half-life which is necessary for T3 induction of the spot 14 gene.
机译：研究了在大鼠肝脏中快速响应3,5,3'-三碘代-L-甲状腺素（T3）诱导的基因点14的调控，以此作为探索甲状腺激素作用的分子基础的模型。肌内注射T3后诱导核前体点14 mRNA表达的时间过程显示了非常短的10至20分钟之间的滞后时间。这种作用的迅速性提示基因表达的诱导是对激素-受体相互作用的主要反应。 T3处理前30分钟注射的蛋白质合成抑制剂环己酰亚胺完全阻断了核前体RNA的积累。盐酸艾美替丁（Emetine）是一种蛋白质合成抑制剂，其作用机理与环己酰亚胺不同，它还阻断了斑点14核前体RNA的诱导。 T3处理后观察到的斑点14基因转录的增加速率（通过核运行分析测定）在存在环己酰亚胺的情况下同样被完全消除了。此外，需要进行蛋白质合成以将斑点14核前体RNA维持在先前用T3处理过的动物中的诱导水平。另一方面，在所研究的45分钟内，环己酰亚胺对T3的吸收或与核受体的结合没有影响。诱导快速动力学的悖论和正在进行的蛋白质合成的要求可以用半衰期极短的蛋白质解释，该蛋白质半衰期非常短，这对于斑点3基因的T3诱导是必需的。

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