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首页> 外文期刊>Molecular and Cellular Endocrinology >The short heterodimer partner receptor differentially modulates peroxisome proliferator-activated receptor alpha-mediated transcription from the peroxisome proliferator-response elements of the genes encoding the peroxisomal beta-oxidation enzymes ac
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The short heterodimer partner receptor differentially modulates peroxisome proliferator-activated receptor alpha-mediated transcription from the peroxisome proliferator-response elements of the genes encoding the peroxisomal beta-oxidation enzymes ac

机译：短异源二聚体伴侣受体差异地调节过氧化物酶体增殖物激活受体的介导转录，该转录是由编码过氧化物酶体β-氧化酶ac的基因的过氧化物酶体增殖物反应元件引起的。

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摘要

The promoter regions of the genes encoding the first two enzymes of the peroxisomal beta-oxidation pathway, acyl-CoA oxidase (AOx) and enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase (HD), contain transcriptional regulatory sequences termed peroxisome proliferator-response elements (PPRE) that are bound by the peroxisome proliferator-activated receptor alpha (PPARalpha) and 9-cis-retinoic acid receptor (RXRalpha) heterodimeric complex. In this study, the role of the short heterodimer partner (SHP) receptor in modulating PPARalpha-mediated gene transcription from the PPREs of the genes encoding AOx and HD was investigated both in vitro and in vivo. In vitro binding assays using glutathione-S-transferase-tagged chimeric receptors for PPARalpha and SHP were used to verify the interaction between PPARalpha and SHP. This interaction was unaffected by the presence of the peroxisome proliferator, Wy-14,643. SHP has been proposed to act as a negative regulator of nuclear hormone receptor activity, and SHP inhibited transcription by PPARalpha/RXRalpha heterodimers from the AOx-PPRE. Surprisingly, SHP potentiated transcription by PPARalpha/RXRalpha heterodimers from the HD-PPRE. This is the first demonstration of positive transcriptional activity attributable to SHP. Together, these results suggest that SHP can modulate PPARalpha/RXRalpha-mediated transcription in a response element-specific manner.
机译：编码过氧化物酶体β-氧化途径的前两种酶的基因的启动子区域，酰基辅酶A氧化酶（AOx）和烯酰基辅酶A水合酶/ 3-羟酰基辅酶A脱氢酶（HD），包含称为过氧化物酶体增殖物的转录调控序列。过氧化物酶体增殖物激活受体α（PPARalpha）和9-顺-视黄酸受体（RXRalpha）异二聚体复合物结合的应答元件（PPRE）。在这项研究中，在体内和体外研究了短异源二聚体伴侣（SHP）受体在调节PPARalpha介导的编码AOx和HD的基因的PPRE的基因转录中的作用。使用谷胱甘肽-S-转移酶标记的嵌合受体对PPARalpha和SHP进行体外结合测定，以验证PPARalpha和SHP之间的相互作用。这种相互作用不受过氧化物酶体增殖物Wy-14643的存在的影响。已经提出，SHP充当核激素受体活性的负调节剂，并且SHP抑制了AOx-PPRE中PPARalpha / RXRalpha异二聚体的转录。令人惊讶的是，SHP增强了HD-PPRE中PPARalpha / RXRalpha异二聚体的转录。这是可归因于SHP的积极转录活性的首次证明。总之，这些结果表明SHP可以以响应元件特异性的方式调节PPARalpha / RXRalpha介导的转录。

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