首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Molecular Characterization of PGC-1β (PPAR Gamma Coactivator 1β) and its Roles in Mitochondrial Biogenesis in Blunt Snout Bream (Megalobrama amblycephala)
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Molecular Characterization of PGC-1β (PPAR Gamma Coactivator 1β) and its Roles in Mitochondrial Biogenesis in Blunt Snout Bream (Megalobrama amblycephala)

机译:PGC-1β(PPARγ激活因子1β)的分子表征及其在钝嘴鼻am(Megalobrama amblycephala)的线粒体生物发生中的作用

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摘要

This study aimed at achieving the molecular characterization of peroxisome proliferator-activated receptor-gamma coactivator 1β (PGC-1β) and exploring its modulatory roles in mitochondria biogenesis in blunt snout bream ( ). A full-length cDNA of was cloned from liver which covered 3110 bp encoding 859 amino acids. The conserved motifs of PGC-1β family proteins were gained by MEME software, and the phylogenetic analyses showed motif loss and rearrangement of in fish. The function of PGC-1β was evaluated through overexpression and knockdown of PGC-1β in primary hepatocytes of blunt snout bream. We observed overexpression of along with enhanced mitochondrial transcription factor A ( ) expression and mtDNA copies in hepatocytes, and its knockdown led to slightly reduced expression. However, knockdown of PGC-1β did not significantly influence expression or mtDNA copies. The alterations in mitochondria biogenesis were assessed following high-fat intake, and the results showed that it induces downregulation of . Furthermore, significant decreases in mitochondrial respiratory chain activities and mitochondria biogenesis were observed by high-fat intake. Our findings demonstrated that overexpression of PGC-1β induces the enhancement of TFAM expression and mtDNA amount but not NRF-1. Therefore, it could be concluded that PGC-1β is involved in mitochondrial biogenesis in blunt snout bream but not through PGC-1β/NRF-1 pathway.
机译:这项研究旨在实现过氧化物酶体增殖物激活的受体-γ共激活因子1β(PGC-1β)的分子表征,并探索其在钝嘴鼻鱼线粒体生物发生中的调节作用。从肝脏克隆了全长cDNA,全长3110 bp,编码859个氨基酸。通过MEME软件获得了PGC-1β家族蛋白的保守基序,系统进化分析表明鱼中基序的丢失和重排。通过钝嘴鲷的原代肝细胞中PGC-1β的过表达和敲低来评估PGC-1β的功能。我们观察到肝细胞中过表达以及增强的线粒体转录因子A()表达和mtDNA拷贝,其敲低导致表达略有降低。但是,PGC-1β的敲低并不显着影响表达或mtDNA拷贝。高脂摄入后评估线粒体生物发生的变化,结果表明它诱导了线粒体的下调。此外,通过高脂摄入可观察到线粒体呼吸链活性和线粒体生物发生显着减少。我们的发现表明,PGC-1β的过表达诱导TFAM表达和mtDNA量的增强,但不诱导NRF-1的增强。因此,可以得出结论,PGC-1β参与钝嘴鲷的线粒体生物发生,但不通过PGC-1β/ NRF-1途径参与。

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