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首页> 外文期刊>The biochemical journal >The effect of phenobarbitone on protein synthesis by liver polyribosomes in fed and starved rats
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The effect of phenobarbitone on protein synthesis by liver polyribosomes in fed and starved rats

机译:苯巴比妥酮对饥饿和饥饿大鼠肝脏核糖体蛋白质合成的影响。

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p1. The effect of phenobarbitone on the rate of protein synthesis and on the sedimentation patterns of various liver subcellular fractions containing ribosomes was studied in rats. 2. Phenobarbitone treatment increased the incorporation of [114C]leucine into protein by all preparations, provided they had not been subjected to preliminary treatment with Sephadex G-25. The phenobarbitone-induced effect on incorporation was associated with a gain in liver weight and a higher degree of polyribosomal aggregation. 3. Preparations that were treated with Sephadex G-25 incorporated more radioactivity into protein, but did not show the response to phenobarbitone treatment. 4. When the influence of starvation and phenobarbitone was studied separately on membrane-bound and membrane-free polyribosomes, it was shown that whereas both classes of polyribosomes were affected by starvation, apparently only the former class was susceptible to phenobarbitone stimulation of protein synthesis. 5. The decreased capacity for protein synthesis of polyribosomes from starved rats was independent of their association with the membranes of the endoplasmic reticulum, but resulted from polyribosomal disaggregation, from an intrinsic defect of the polyribosomes themselves and from changes in composition of the cell cap. 6. The results are discussed in relation to the problem of the control of protein biosynthesis and of the functional separation of membrane-bound and membrane-free polyribosomes./p
机译:> 1。在大鼠中研究了苯巴比妥酮对蛋白质合成速率以及含有核糖体的各种肝亚细胞级分沉降模式的影响。 2.苯巴比妥治疗可提高所有制剂中[114C]亮氨酸向蛋白质中的掺入,条件是未对它们进行Sephadex G-25的初步处理。苯巴比妥诱导的掺入作用与肝脏重量增加和多核糖体聚集程度增加有关。 3.用Sephadex G-25处理的制剂将更多的放射性掺入蛋白质中,但未显示出对苯巴比妥治疗的反应。 4.当分别研究饥饿和苯巴比妥对膜结合的和无膜的多核糖体的影响时,表明虽然两类多核糖体都受饥饿影响,但显然只有前一类易受苯巴比妥刺激蛋白质合成。 5.饥饿的大鼠的多核糖体的蛋白质合成能力降低,与它们与内质网膜的结合无关,但是由于多核糖体解体,多核糖体本身的固有缺陷以及细胞帽组成的变化所致。 6.讨论了有关蛋白质生物合成的控制以及膜结合的和无膜的多核糖体功能分离问题的结果。

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