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Regulation of translation factors during hindlimb unloading and denervation of skeletal muscle in rats.

机译:大鼠后肢卸载和骨骼肌神经失调期间翻译因子的调节。

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摘要

In the rat, denervation and hindlimb unloading are two commonly employed models used to study skeletal muscle atrophy. In these models, muscle atrophy is generally produced by a decrease in protein synthesis and an increase in protein degradation. The decrease in protein synthesis has been suggested to occur by an inhibition at the level of protein translation. To better characterize the regulation of protein translation, we investigated the changes that occur in various translation initiation and elongation factors. We demonstrated that both hindlimb unloading and denervation produce alterations in the phosphorylation and/or total amount of the 70-kDa ribosomal S6 kinase, eukaryotic initiation factor 2 alpha-subunit, and eukaryotic elongation factor 2. Our findings indicate that the regulation of these protein translation factors differs between the models of atrophy studied and between the muscles evaluated (e.g., soleus vs. extensor digitorum longus).
机译:在大鼠中,去神经作用和后肢卸载是用于研究骨骼肌萎缩的两种常用模型。在这些模型中,肌肉萎缩通常是由于蛋白质合成减少和蛋白质降解增加而产生的。已经提出蛋白质合成的减少是通过抑制蛋白质翻译水平而发生的。为了更好地表征蛋白质翻译的调控,我们研究了各种翻译起始和延伸因子中发生的变化。我们证明后肢卸载和去神经都产生磷酸化和/或70 kDa核糖体S6激酶,真核起始因子2α亚基和真核延伸因子2的总量变化。我们的发现表明,这些蛋白质的调控在研究的萎缩模型之间和在所评估的肌肉之间,翻译因子有所不同(例如,比目鱼肌与趾长伸肌)。

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