人WRAP53基因启动子区的生物信息学分析
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摘要
人WRAP53基因隶属于WD重复蛋白家族,被发现在端粒酶的组装、卡哈尔体的形成和DNA损伤的修复等过程中发挥着重要作用,但WRAP53基因表达调控的分子机制尚不明确.利用生物信息学软件对人WRAP53基因近端启动子-2 000 bp～-1 bp区域的结构特征、转录因子结合位点和CpG岛进行预测分析.Promotor 2.0和NNPP均预测出人WRAP53β基因有2个启动子;JASPAR和AliBaba 2.1发现有众多转录因子潜在结合位点存在该序列上;CpG Plot、CpG Finder和MethPrimer软件均预测出人WRAP53基因启动子-2 000 bp～-1 bp区域存在1个CpG岛.对人WRAP53基因启动子区开展的生物信息学分析,有助于了解该基因启动子区的结构和功能,为后续开展人WRAP53基因表达调控机制研究奠定了基础.
Human WRAP53 gene, belongs the family of WD repeat protein, and plays a critical role in the assemble of telomerase, formation of Cajal body and DNA damage and repair. However, the potential regulation mechanism of WRAP53 gene expression is still unclear. The human WRAP53 gene's promotor region-2 000 bp ～-1 bp are used to analyze by some online bioinformatics tools to obtain the characteristics of the promoter, transcription factor binding site and CpG island. The same number of promoters predicted by Promotor 2.0 and NNPP were 2. Two promoters of human WRAP53 gene have been predicted by both Promotor 2.0 and NNPP. Many potential transcription factor binding sites have been found by JASPAR and AliBaba 2.1. The existence of 1 CpG island in the region of-2 000 bp ～-1 bp promoter of human WRAP53 gene was predicted by CpG Plot, CpG Finder and MethPrimer software. The bioinformatics analysis of the human WRAP53 gene region can provide significant information for the structure and function of the gene promoter, and lay a foundation for the subsequent research on the regulation mechanism of human WRAP53 gene expression.
Human WRAP53 gene, belongs the family of WD repeat protein, and plays a critical role in the assemble of telomerase, formation of Cajal body and DNA damage and repair. However, the potential regulation mechanism of WRAP53 gene expression is still unclear. The human WRAP53 gene's promotor region-2 000 bp ～-1 bp are used to analyze by some online bioinformatics tools to obtain the characteristics of the promoter, transcription factor binding site and CpG island. The same number of promoters predicted by Promotor 2.0 and NNPP were 2. Two promoters of human WRAP53 gene have been predicted by both Promotor 2.0 and NNPP. Many potential transcription factor binding sites have been found by JASPAR and AliBaba 2.1. The existence of 1 CpG island in the region of-2 000 bp ～-1 bp promoter of human WRAP53 gene was predicted by CpG Plot, CpG Finder and MethPrimer software. The bioinformatics analysis of the human WRAP53 gene region can provide significant information for the structure and function of the gene promoter, and lay a foundation for the subsequent research on the regulation mechanism of human WRAP53 gene expression.
引文
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[3] Sofia H,Hanif R,Elisabeth H,et al.The scaffold protein WRAP53β orchestrates the ubiquitin response critical for DNA doublestrand break repair[J].Genes & Development,2014,28(24):2726-2738.
[4] Zhong F,Savage S A,Shkreli M,et al.Disruption of telomerase trafficking by TCAB1 mutation causes dyskeratosis congenita[J].Genes & Development,2011,25(1):11-16.
[5] Sun C K,Luo X B,Gou Y P,et al.TCAB1:a potential target for diagnosis and therapy of head and neck carcinomas[J].Molecular Cancer,2014,13(1):1-12.
[6] Garvin S,Tiefenbock K,Farnebo L,et al.Nuclear expressionof WRAP53β is associated with a positive response to radiotherapy and improved overall survival in patients with head and neck squamous cell carcinoma[J].Oral Oncology,2015,51(1):24-30.
[7] Mahmoudi S,Henriksson S,Corcoran M,et al.WRAP53,a natural p53 antisense transcript required for p53 induction upon DNA damage[J].Molecular Cell,2009,33(4):462-471.
[8] Mahmoudi S,Henriksson S,Farnebo L,et al.WRAP53 promotes cancer cell survival and is a potential target for cancer therapy[J].Cell Death Dis,2011,2:114.
[9] Sun Y,Yang C,Chen J,et al.Overexpression of WDR79 in nonsmall cell lung cancer is linked to tumour progression[J].Journal of Cellular & Molecular Medicine,2016,20(4):698-709.
[10] Merlo A,Herman JG,Mao L,et al.5' CpG island methylation is associated with transcriptional silencing of the tumour suppressor p16/CDKN2/MTS1 in human cancers[J].Nat Med,1995,1(7):686-92.