Integration of a c-myc transgene results in disruption of the mouse Gtf2ird1 gene, the homologue of the human GTF2IRD1 gene hemizygously deleted in Williams-Beuren syndrome.

Durkin ME; Keck-Waggoner CL; Popescu NC; Thorgeirsson SS

首页> 外文期刊>Genomics >Integration of a c-myc transgene results in disruption of the mouse Gtf2ird1 gene, the homologue of the human GTF2IRD1 gene hemizygously deleted in Williams-Beuren syndrome.

【24h】

Integration of a c-myc transgene results in disruption of the mouse Gtf2ird1 gene, the homologue of the human GTF2IRD1 gene hemizygously deleted in Williams-Beuren syndrome.

机译：c-myc转基因的整合导致小鼠Gtf2ird1基因的破坏，该基因是在Williams-Beuren综合征中半合删除的人GTF2IRD1基因的同源物。

获取原文

获取原文并翻译 | 示例

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

文献代查 >>

页面导航

摘要
著录项
相似文献
相关主题

摘要

Transgenic mice expressing c-myc under the control of the albumin promoter and enhancer develop liver tumors and have served as a useful model for studying the progression of hepatocarcinogenesis. The chromosomes of one line of c-myc transgenic mice carry the reciprocal translocation t(5;6)(G1;F2) adjacent to the transgene insertion site on the 5G1-ter segment translocated to chromosome 6. To characterize the genomic alterations in the c-myc transgenic animals, we have cloned the mouse DNA flanking the transgene array. By linkage mapping, the transgene integration site was localized to the region of distal chromosome 5 syntenic to the region on human chromosome 7q11.23 that is hemizgygously deleted in Williams-Beuren syndrome, a multisystemic developmental disorder. Comparison of the genomic DNA structure in wildtype and transgenic mice revealed that the transgene integration had induced an approximately 40-kb deletion, starting downstream of the Cyln2 gene and including the first exon of the Gtf2ird1 gene. Gtf2ird1 encodes a polypeptide related to general transcription factor TFII-I, and it is the mouse orthologue of GTF2IRD1 (WBSCR11), one of the genes commonly deleted in Williams-Beuren syndrome patients. Loss of the 5' end of the Gtf2ird1 gene resulted in greatly reduced expression of Gtf2ird1 mRNA in mice homozygous for the transgene.

机译：在白蛋白启动子和增强子的控制下表达c-myc的转基因小鼠发展为肝肿瘤，并已成为研究肝癌发生发展的有用模型。一行c-myc转基因小鼠的染色体携带相互易位的t（5; 6）（G1; F2），其与转位至6号染色体的5G1-ter区段上的转基因插入位点相邻。 c-myc转基因动物，我们已经克隆了转基因阵列两侧的小鼠DNA。通过连锁作图，将转基因整合位点定位在与人类染色体7q11.23上同义缺失的远端染色体5号区域上，该区域在多系统发育性疾病Williams-Beuren综合征中被半删除。比较野生型和转基因小鼠中的基因组DNA结构，发现转基因整合已诱导了大约40 kb的缺失，从Cyln2基因的下游开始，包括Gtf2ird1基因的第一个外显子。 Gtf2ird1编码与一般转录因子TFII-1相关的多肽，它是GTF2IRD1（WBSCR11）的小鼠直系同源基因，它是Williams-Beuren综合征患者中通常缺失的基因之一。 Gtf2ird1基因5'末端的丢失导致纯合转基因小鼠的Gtf2ird1 mRNA表达大大降低。

著录项

来源
《Genomics》 |2001年第1期|共8页
作者
Durkin ME; Keck-Waggoner CL; Popescu NC; Thorgeirsson SS;
展开▼
作者单位

展开▼
收录信息
原文格式 PDF
正文语种 eng
中图分类遗传学;
关键词
Genes; myc; Transcription Factors; Williams Syndrome; GTF2IRD1-protein; RNA; Messenger; 基因; MYC; 转录因子; 威廉斯综合征;

机译：Genes;myc;Transcription Factors;Williams Syndrome;GTF2IRD1-protein;RNA;Messenger;基因;MYC;转录因子;威廉斯综合征;

相似文献

外文文献
中文文献
专利

1. Integration of a c-myc transgene results in disruption of the mouse Gtf2ird1 gene, the homologue of the human GTF2IRD1 gene hemizygously deleted in Williams-Beuren syndrome. [J] . Durkin ME, Keck-Waggoner CL, Popescu NC, Genomics . 2001,第1期

机译：c-myc转基因的整合导致小鼠Gtf2ird1基因的破坏，该基因是在Williams-Beuren综合征中半合删除的人GTF2IRD1基因的同源物。
2. Genomic organization of the genes Gtf2ird1, Gtf2i, and Ncf1 at the mouse chromosome 5 region syntenic to the human chromosome 7q11.23 Williams syndrome critical region. [J] . Bayarsaihan D, Dunai J, Greally JM, Genomics . 2002,第1期

机译：Gtf2ird1，Gtf2i和Ncf1基因的基因组组织在与人染色体7q11.23 Williams综合征关键区域同义的小鼠5号染色体区域上。
3. An In Vivo Gain-of-Function Screen Identifies the Williams-Beuren Syndrome Gene GTF2IRD1 as a Mammary Tumor Promoter [J] . Yongliang Huo, Timothy Su, Qiuyin Cai, Cell Reports . 2016,第10期

机译：体内功能增益屏幕将Williams-Beuren综合征基因GTF2IRD1鉴定为乳腺肿瘤启动子
4. Recombinant AAV Vectors as Natural Nanoparticles Caused Global and Stable Transgene Expression in Mouse Brain by Intravenous Administration [C] . Hongwei Zhang, Bin Yang, Guangping Gao Annual meeting exposition of the Controlled Release Society . 2011

机译：重组AAV载体作为天然纳米粒子通过静脉给药引起小鼠脑中全局和稳定的转基因表达
5. Diverse mechanisms of human genetic disease: Splice order determination in the COL1A2 gene. Effects that influence splice site mutations in osteogenesis imperfecta and a translocation disrupting SNRPN gene causes Prader-Willi syndrome. [D] . Kuslich, Christine D. 1999

机译：人类遗传疾病的多种机制：COL1A2基因的剪接顺序确定。影响成骨不全症中剪接位点突变和易位破坏SNRPN基因的效应会导致Prader-Willi综合征。
6. An in vivo gain-of-function screen identifies the Williams-Beuren Syndrome gene GTF2IRD1 as a mammary tumor promoter [O] . Yongliang Huo, Timothy Su, Qiuyin Cai, -1

机译：体内功能获得筛选将Williams-Beuren综合征基因GTF2IRD1确定为乳腺肿瘤启动子
7. An In Vivo Gain-of-Function Screen Identifies the Williams-Beuren Syndrome Gene GTF2IRD1 as a Mammary Tumor Promoter [O] . Huo Yongliang, Su Timothy, Cai Qiuyin, 2016

机译：体内功能获取屏幕将Williams-Beuren综合征基因GTF2IRD1鉴定为乳腺肿瘤促进剂

Integration of a c-myc transgene results in disruption of the mouse Gtf2ird1 gene, the homologue of the human GTF2IRD1 gene hemizygously deleted in Williams-Beuren syndrome.

摘要

著录项

相似文献

相关主题

期刊订阅