Global proteomic profiling of the uniquely human CHRFAM7A gene in transgenic mouse brain
Global proteomic profiling of the uniquely human CHRFAM7A gene in transgenic mouse brain
复制标题
转基因小鼠大脑中独特的人类 CHRFAM7A 基因的整体蛋白质组学分析
DOI：
10.1016/j.gene.2019.143996
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发表时间：
2019-09-25
期刊：
影响因子：
3.5
通讯作者：
Dang, Xitong
中科院分区：
文献类型：
--
作者：
Jiang, Yu;Yuan, Haiyang;Dang, Xitong
人类特有的α 7-nAChR基因（CHRFAM 7A）是由两个部分重复的基因FAM 7和α 7-nAChR基因（CHRNA 7）融合而成的，并插入在CHRNA 7基因的同一条染色体5'端。CHRFAM 7A基因转录后产生一个1256 bp的开放阅读框，编码dup-α 7-nAChR，其中α 7-nAChR的N-末端配体结合域的146个氨基酸残基被FAM 7的27个氨基酸残基取代。在体外，dup-alpha 7-nAChR已被证明与alpha 7-nAChR形成异源五聚体，并显性负调控alpha 7-nAChR的通道功能。然而，CHRFAM 7A基因对体内脑中α 7-nAChR生物学的贡献在很大程度上仍然是一个推测问题。建立CHRFAM 7A转基因小鼠，并使用iTRAQ-2D-LC-MS/MS蛋白质组学技术分析全脑差异表达的蛋白质。倍数变化>= 1.2或
The uniquely human alpha 7-nAChR gene (CHRFAM7A) is evolved from the fusion of two partially duplicated genes, FAM7 and alpha 7-nAChR gene (CHRNA7), and is inserted on same chromosome 15, 5' end of the CHRNA7 gene. Transcription of CHRFAM7A gene produces a 1256-bp open reading frame encoding dup-alpha 7-nAChR, where a 27aminoacid residues from FAM7 replaced the 146-aminoacid residues of the N-terminal extracellular ligand binding domain of alpha 7-nAChR. In vitro, dup-alpha 7-nAChR has been shown to form hetero-pentamer with alpha 7-nAChR and dominant-negatively regulates the channel functions of alpha 7-nAChR. However, the contribution of CHRFAM7A gene to the biology of alpha 7-nAChR in the brain in vivo remains largely a matter of conjecture. CHRFAM7A transgenic mouse was created and differentially expressed proteins were profiled from the whole brain using iTRAQ-2D-LC-MS/MS proteomic technology. Proteins with a fold change of >= 1.2 or