Ube3a-ATS截断激活父本Ube3a并改善安格尔曼综合征小鼠模型行为缺陷

资源简介

Ube3a-ATS截断激活父本Ube3a并改善安格尔曼综合征小鼠模型行为缺陷

【数据集背景】

本数据集源站标题为《Truncation of Ube3a-ATS Unsilences Paternal Ube3a and Ameliorates Behavioral Defects in the Angelman Syndrome Mouse Model》。配套论文《Truncation of Ube3a-ATS Unsilences Paternal Ube3a and Ameliorates Behavioral Defects in the Angelman Syndrome Mouse Model》发表于 PLoS Genetics（2013），DOI：10.1371/journal.pgen.1004039。源站首次发布：2013-12-26。

【数据内容】

源站原始描述：Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by maternal deficiency of the imprinted gene UBE3A. Individuals with AS suffer from intellectual disability, speech impairment, and motor dysfunction. Currently there is no cure for the disease. Here, we evaluated the phenotypic effect of activating the silenced paternal allele of Ube3a by depleting its antisense RNA Ube3a-ATS in mice. Premature termination of Ube3a-ATS by poly(A) cassette insertion activates expression of Ube…

【数据结构与技术规格】

文件数 11 个，合计 10.51 MB。Figure_S1.tif：image/tiff，1.05 MB。Figure_S3.tif：image/tiff，901.82 KB。数据集 DOI：10.1371/journal.pgen.1004039。

【主题与分类】

源站学科分类：Biological Sciences。主题标签：truncation、unsilences、paternal、ameliorates、defects、angelman。

【适用方向】

源站学科分类标注为 Biological Sciences。

【获取与许可】

源站页面：https://plos.figshare.com/articles/dataset/Truncation_of_Ube3a_ATS_Unsilences_Paternal_Ube3a_and_Ameliorates_Behavioral_Defects_in_the_Angelman_Syndrome_Mouse_Model/887095

使用许可：CC BY 4.0（https://creativecommons.org/licenses/by/4.0/）。

规范引用：Meng, Linyan; Erwin Person, Richard; Huang, Wei; Jun Zhu, Ping; Costa-Mattioli, Mauro; L. Beaudet, Arthur (2016). Truncation of Ube3a-ATS Unsilences Paternal Ube3a and Ameliorates Behavioral Defects in the Angelman Syndrome Mouse Model. PLOS Genetics. Dataset

【使用注意】

· 源站最后修改于 2023-06-04，引用时请注意版本时效。