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首页> 外文期刊>Cellular Signalling >Signalling pathways in the induction of proteasome expression by proteolysis-inducing factor in murine myotubes
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Signalling pathways in the induction of proteasome expression by proteolysis-inducing factor in murine myotubes

机译：蛋白水解诱导因子在鼠肌管中诱导蛋白酶体表达的信号通路

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The mechanism by which the tumour product proteolysis-inducing factor (PIF) induced increased expression of the ubiquitin-proteasome proteolytic pathway was studied in C2C12 murine myotubes. PIF directly increased total protein breakdown at concentrations between 4 and 16 nM, and the effect was attenuated by eicosapentaenoic acid (EPA) and the 12/15-lipoxygenase inhibitor 2,3,5-trimethyl-6-(3-pyridylmethyl)1,4-benzoquinone (CV-6504). PIF induced an increased expression of mRNA for proteasome alpha (C2) and beta (C5) subunits over the same concentration range as that inducing protein degradation and with a maximal effect 4 h after PIF addition. The effect was attenuated by both EPA and CV-6504, suggesting the role of a lipoxygenase metabolite in the increased gene transcription. 15(S)-Hydroxyeicosatetraenoic acid [15(S)-HETE], an intermediate in intracellular signalling by PIF was shown to activate protein kinase Calpha(PKC) over the same concentration range as that inducing proteasome expression and both effects were attenuated by calphostin C, a highly specific inhibitor of PKC. 15(S)-HETE induced phosphorylation and degradation of IkappaBalpha at the same concentrations as those inducing 20S proteasome expression, and this effect was attenuated by calphostin C, suggesting the mediation of PKC. These results suggest potential control points in proteasome activation that could be useful for therapeutic intervention. (C) 2004 Elsevier Inc. All rights reserved.
机译：在C2C12鼠肌管中研究了肿瘤产物蛋白水解诱导因子（PIF）诱导泛素-蛋白酶体蛋白水解途径表达增加的机制。 PIF在4至16 nM的浓度下直接增加了总蛋白质分解，并且二十碳五烯酸（EPA）和12 / 15-脂氧合酶抑制剂2,3,5-三甲基-6-（3-吡啶基甲基）1减弱了这种作用， 4-苯醌（CV-6504）。在与诱导蛋白质降解相同的浓度范围内，PIF诱导蛋白酶体α（C2）和β（C5）亚基的mRNA表达增加，并且在添加PIF后4 h发挥最大作用。 EPA和CV-6504均减弱了这种作用，表明脂氧合酶代谢产物在基因转录增加中的作用。 15（S）-羟基二十碳四烯酸[15（S）-HETE]（通过PIF进行细胞内信号传导的中间体）在与诱导蛋白酶体表达相同的浓度范围内激活蛋白激酶Calpha（PKC），钙磷蛋白减弱了这两种作用C，PKC的高度特异性抑制剂。 15（S）-HETE以与诱导20S蛋白酶体表达相同的浓度诱导IkappaBalpha的磷酸化和降解，钙磷蛋白C减弱了这种作用，表明PKC的介导作用。这些结果表明蛋白酶体激活的潜在控制点可能对治疗干预有用。 （C）2004 Elsevier Inc.保留所有权利。

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