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蛋白质缺乏小鼠重新喂食后肝脏RNA聚合酶I激活的调控。

Control of activation of liver RNA polymerase I occurring after re-feeding of protein-depleted mice.

作者信息

Haim L, Iapalucci-Espinoza S, Conde R, Franze-Fernández M T

出版信息

Biochem J. 1983 Mar 15;210(3):837-44. doi: 10.1042/bj2100837.

Abstract

Shortly after feeding protein-depleted mice with a meal containing protein, the RNA polymerase I activity in isolated liver nuclei shows a 2-fold increase over the values in the nuclei of either normal or protein-depleted mice. The activity of the RNA polymerase I solubilized from nuclei of re-fed mice was slightly enhanced, probably reflecting an increase in enzyme amount. However, this increase only accounts for about 30% of the stimulation of transcription in the intact nuclei. Administration of pactamycin, an inhibitor of protein synthesis, to normal or protein-depleted mice has almost no inhibitory effect on the RNA polymerase I activity in the isolated nuclei. On the contrary, within 15 min after treatment with the drug, the stimulated activity in nuclei from re-fed mice declines towards the values in normal or protein-depleted mice and then remains constant. The activity of the solubilized enzyme remains slightly elevated for at least 2 1/2 h after re-fed mice are treated with pactamycin. These observations indicate that the stimulation of the RNA polymerase I activity in the intact nuclei after re-feeding is controlled by mechanisms other than an increase in the enzyme amount and suggest the presence of short-lived proteins required for inducing an activated state of transcription.

摘要

用含蛋白质的一餐喂食蛋白质缺乏的小鼠后不久,分离的肝细胞核中的RNA聚合酶I活性比正常或蛋白质缺乏小鼠细胞核中的值增加了2倍。从再喂食小鼠的细胞核中溶解的RNA聚合酶I的活性略有增强,这可能反映了酶量的增加。然而,这种增加仅占完整细胞核中转录刺激的约30%。给正常或蛋白质缺乏的小鼠施用蛋白质合成抑制剂放线菌酮,对分离细胞核中的RNA聚合酶I活性几乎没有抑制作用。相反,在用该药物处理后15分钟内,再喂食小鼠细胞核中的刺激活性向正常或蛋白质缺乏小鼠中的值下降,然后保持恒定。在用放线菌酮处理再喂食小鼠后,溶解酶的活性至少在2.5小时内仍略有升高。这些观察结果表明,再喂食后完整细胞核中RNA聚合酶I活性的刺激是由酶量增加以外的机制控制的,并提示存在诱导转录激活状态所需的短寿命蛋白质。

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