论文部分内容阅读
脆性X综合征(FXS)是一种遗传性智力低下疾病,其发病率仅次于21三体综合征.脆性X智力低下蛋白(FMRP)是FXS的关键性致病因子,该蛋白由脆性X智力低下基因1(FMR1)编码所得.FMR1在神经肌肉和睾丸组织中广泛表达.脆性X相关蛋白1(FXR1P)则是由FMR1的同源基因脆性X相关基因1(FXR1)编码所得,并且与蛋白质和RNAs之间存在着相互作用.许多疾病都涉及到FXR1表达的改变.为了了解FXR1P与CMAS(胞嘧啶单核苷酸-N-乙酰神经氨酸合成酶)相互作用所产生的的生物学效应,我们构建了FXR1的过表达载体,并观察其在PC12细胞(大鼠鼠肾上腺嗜铬细胞瘤细胞)和VSMC(血管平滑肌细胞)中的表达以及继而对于细胞形态和CMAS活性相关的许多细胞指标的效应.我们证实,FXR1基因的过表达可以提高PC12细胞中CMAS的活性,并对于该类细胞的生长提供一定程度的保护作用.PC12细胞是一种较为常见的用于研究神经系统疾病的细胞系.结论:我们推测FXR1P是一个组织特异调节因子,可以改变PC12细胞而非VSMC细胞中神经节苷酯(GM1)的浓度.
Fragile X syndrome (FXS) is a hereditary mental retardation disorder with the morbidity second only to trisomy 21. Fragile X mental retardation protein (FMRP) is a key virulence factor for FXS and consists of fragile X (FMR1), which is widely expressed in neuromuscular and testicular tissues.Fragile X-related protein 1 (FXR1P) is encoded by the FMR1 homologous gene Fragile X-related gene 1 (FXR1) Interactions exist between proteins and RNAs Many diseases involve changes in FXR1 expression To understand the biology of the interaction of FXR1P with CMAS (cytosine monophosphate-N-acetylneuraminic acid synthetase) Effect, we constructed an overexpression vector for FXR1 and observed its expression in PC12 cells (rat rat adrenal pheochromocytoma cells) and VSMC (vascular smooth muscle cells), followed by many of the cells associated with cell morphology and CMAS activity We confirmed that FXR1 gene overexpression can increase the activity of CMAS in PC12 cells and provide some protection for the growth of these cells.PC12 cells are a kind of common method used to study the nervous system Disease cell lines Conclusion: We speculate FXR1P is a tissue specific regulatory factor can be changed instead of the concentration of PC12 cells VSMC cells ganglioside (GM1) of.