Global loss of imprinting leads to widespread tumorigenesis in adult mice.

Holm TM; Jackson Grusby L; Brambrink T; Yamada Y; Rideout WM 3rd; Jaenisch R

首页> 外文期刊>Cancer Cell >Global loss of imprinting leads to widespread tumorigenesis in adult mice.

【24h】

Global loss of imprinting leads to widespread tumorigenesis in adult mice.

机译：整体印迹的丧失导致成年小鼠中广泛的肿瘤发生。

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

Loss of imprinting (LOI), commonly observed in human tumors, refers to loss of monoallelic gene regulation normally conferred by parent-of-origin-specific DNA methylation. To test the function of LOI in tumorigenesis, we developed a model by using transient demethylation to generate imprint-free mouse embryonic stem cells (IF-ES cells). Embryonic fibroblasts derived from IF-ES cells (IF-MEFs) display TGFbeta resistance and reduced p19 and p53 expression and form tumors in SCID mice. IF-MEFs exhibit spontaneous immortalization and cooperate with H-Ras in cellular transformation. Chimeric animals derived from IF-ES cells develop multiple tumors arising from the injected IF-ES cells within 12 months. These data demonstrate that LOI alone can predispose cells to tumorigenesis and identify a pathway through which immortality conferred by LOI lowers the threshold for transformation.

机译：通常在人类肿瘤中观察到的印记丧失（LOI）是指通常由起源母体特异性DNA甲基化赋予的单等位基因调节的丧失。为了测试LOI在肿瘤发生中的功能，我们开发了一个模型，该模型通过使用瞬时去甲基化来生成无印迹的小鼠胚胎干细胞（IF-ES细胞）。源自IF-ES细胞（IF-MEF）的胚胎成纤维细胞显示出TGFbeta耐药性并降低p19和p53表达，并在SCID小鼠中形成肿瘤。 IF-MEF表现出自发的永生化，并在细胞转化中与H-Ras协同作用。衍生自IF-ES细胞的嵌合动物会在12个月内因注射的IF-ES细胞而引起多发肿瘤。这些数据表明，单独的LOI可以使细胞易于发生肿瘤，并确定LOI赋予的永生性降低转化阈值的途径。

著录项

来源
《Cancer Cell》 |2005年第4期|共11页
作者
Holm TM; Jackson Grusby L; Brambrink T; Yamada Y; Rideout WM 3rd; Jaenisch R;
展开▼
作者单位

展开▼
收录信息
原文格式 PDF
正文语种 eng
中图分类肿瘤学;
关键词
embryonic stem cell; tumorigenesis; Laboratory mice; Imprinting (Psychology); 铭记(心理学);

机译：embryonic stem cell;tumorigenesis;Laboratory mice;Imprinting (Psychology);铭记(心理学);

相似文献

外文文献
中文文献
专利

1. Global loss of imprinting leads to widespread tumorigenesis in adult mice. [J] . Holm TM, Jackson Grusby L, Brambrink T, Cancer Cell . 2005,第4期

机译：整体印迹的丧失导致成年小鼠中广泛的肿瘤发生。
2. Early onset amyloid lesions lead to severe neuritic abnormalities and local, but not global neuron loss in APPPS1 transgenic mice. [J] . Rupp NJ, Wegenast Braun BM, Radde R, Neurobiology of Aging: Experimental and Clinical Research . 2011,第12期

机译：早期发作的淀粉样蛋白损伤会导致严重的神经异常和APPPS1转基因小鼠的局部神经元丢失，但不会导致整体神经元丢失。
3. Loss of APC function in mesenchymal cells surrounding the Mullerian duct leads to myometrial defects in adult mice. [J] . Wang Y, Jia Y, Franken P, Molecular and Cellular Endocrinology . 2011,第1a2期

机译：穆勒管周围的间充质细胞中APC功能的丧失会导致成年小鼠的肌层缺损。
4. Synergism between magnetic fields and lead overload on the permeability of the blood brain barrier in mice. [C] . M. Perez-Calvo, B. Ribas-Ozonas International conference on computational methods in electrical engineering and electromagnetics . 2003

机译：磁场之间的协同作用与小鼠血脑屏障渗透性的铅过载。
5. Deletion of the Chromatin Remodeling Factor Brg1 Leads to Genomic Instability During Development, and Confers Sensitivity to Adult-onset Doxorubicin Cardiotoxicity in Mice. [D] . Boyle, Michael Christopher. 2014

机译：染色质重塑因子Brg1的删除导致发育过程中的基因组不稳定，并赋予小鼠成年发作的阿霉素心脏毒性敏感性。
6. Mutation of a Single CTCF Target Site within the H19 Imprinting Control Region Leads to Loss of Igf2 Imprinting and Complex Patterns of De Novo Methylation upon Maternal Inheritance [O] . Vinod Pant, Sreenivasulu Kurukuti, Elena Pugacheva, 2001

机译：H19印迹控制区域内单个CTCF目标位点的突变会导致Igf2印迹的丧失和母体遗传后从头甲基化的复杂模式
7. Global loss of imprinting leads to widespread tumorigenesis in adult mice [O] . Holm Teresa M., Jackson-Grusby Laurie, Brambrink Tobias, 2006

机译：印迹的整体丧失导致成年小鼠广泛的肿瘤发生

Global loss of imprinting leads to widespread tumorigenesis in adult mice.

摘要

著录项

相似文献

相关主题

期刊订阅