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首页> 外文期刊>Life sciences >Hyperphosphorylation of rat liver proteasome subunits: the effects of ethanol and okadaic acid are compared.
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Hyperphosphorylation of rat liver proteasome subunits: the effects of ethanol and okadaic acid are compared.

机译：大鼠肝脏蛋白酶体亚基的过度磷酸化：比较了乙醇和冈田酸的作用。

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In experimental alcoholic liver disease, protein degradation by the ATP-ubiquitin-proteasome pathway is inhibited. Failure of the proteasome to eliminate cytoplasmic proteins leads to the accumulation of oxidized and otherwise modified proteins. One possible explanation for the inhibition of the proteasome is hyperphosphorylation of proteasome subunits. To examine this possibility, the 26S proteasomes from the liver of rats fed ethanol and a pair-fed control were studied by isolating the proteasomes in a purified fraction. The effect of ethanol on the phosphorylation of proteasomal subunits was compared with the hyperphosphorylation of the proteasomes caused by okadaic acid given to rats in vivo. Ethanol ingestion caused an inhibition of the chymotrypsin-like activity of the purified proteasome. The 2D electrophoresis and Western blot analysis of the purified 20S and 26S proteasomes from the ethanol-fed rats indicated that hyperphosphorylation of proteasomal subunits had occured. The proteasomal alpha type subunits C9/alpha3 and C8/alpha7 were hyperphosphorylated compared to the controls. Chymotrypsin-like activity was also inhibited by okadaic acid treatment similar to ethanol feeding. The 26S proteasome fraction examined by isoelectric focusing gel revealed many hyperphosphorylated bands in the proteasomes from the okadaic acid treated and the ethanol fed rat livers compared with the controls. In conclusion hyperphosphorylation of the proteasome subunits occurs in the ethanol treated proteasomal subunits which could be one mechanism of the inhibition of the 26S proteasome caused by ethanol feeding.
机译：在实验性酒精性肝病中，通过ATP泛素-蛋白酶体途径抑制蛋白质降解。蛋白酶体不能消除细胞质蛋白会导致氧化蛋白和修饰蛋白的积累。抑制蛋白酶体的一种可能解释是蛋白酶体亚基的过度磷酸化。为了检验这种可能性，通过分离纯化级分中的蛋白酶体，研究了喂食乙醇和成对喂养的对照大鼠肝脏中的26S蛋白酶体。将乙醇对蛋白酶体亚基磷酸化的影响与体内冈田酸引起的蛋白酶体过磷酸化作用进行了比较。乙醇摄入会抑制纯化的蛋白酶体的胰凝乳蛋白酶样活性。来自乙醇喂养的大鼠的纯化的20S和26S蛋白酶体的2D电泳和Western blot分析表明，蛋白酶体亚基的过度磷酸化已经发生。与对照相比，蛋白酶体α型亚基C9 / alpha3和C8 / alpha7被过度磷酸化。冈田酸处理也类似于乙醇喂养，也抑制了胰凝乳蛋白酶样活性。通过等电聚焦凝胶检测的26S蛋白酶体级分显示，与对照相比，经冈田酸处理和乙醇喂养的大鼠肝脏的蛋白酶体中有许多超磷酸化带。总之，在乙醇处理的蛋白酶体亚基中发生蛋白酶体亚基的过度磷酸化，这可能是抑制由乙醇进料引起的26S蛋白酶体的一种机制。

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