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从硒蛋白到软骨内骨化:一种具有 miRNA 潜力的新机制与骨相关疾病有关?

From selenoprotein to endochondral ossification: a novel mechanism with microRNAs potential in bone related diseases?

机构信息

Department of Genetics and Molecular Biology, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, PR China.

出版信息

Med Hypotheses. 2011 Nov;77(5):807-11. doi: 10.1016/j.mehy.2011.07.042.

Abstract

Selenium participates the formation of selenoprotein as the form of selenocysteine, the active-site residue essential for protein catalytic activity. It has been proved that selenium deficiency leads to the abnormality of selenoprotein biosynthesis, which may lead to disorders of brain, skeleton development and cartilage chondrocyte differentiation. The production of selenoproteins is regulated by selenocysteine insertion sequence (SECIS) and several trans-acting factors in eukaryotic cells. However, the mechanism of posttranscriptional modification of selenoproteins biosynthesis seldom needs to be elucidated. Recent evidence indicates that miRNAs are key points in the process of endochondral ossification. The hypothesis is that the expression of key selenoproteins may regulate directly or indirectly via trans-acting factors by miRNAs during skeleton development.

摘要

硒以硒代半胱氨酸的形式参与硒蛋白的形成,是蛋白质催化活性所必需的活性部位残基。已经证明,硒缺乏会导致硒蛋白生物合成异常,这可能导致脑、骨骼发育和软骨软骨细胞分化障碍。真核细胞中,硒蛋白的产生受硒代半胱氨酸插入序列 (SECIS) 和几种反式作用因子的调节。然而,硒蛋白生物合成的转录后修饰机制尚需阐明。最近的证据表明,miRNAs 是软骨内骨化过程中的关键点。该假说认为,在骨骼发育过程中,关键的硒蛋白的表达可能通过 miRNAs 直接或间接地通过反式作用因子进行调节。

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