The p53-induced lincRNA-p21 derails somatic cell reprogramming by sustaining H3K9me3 and CpG methylation at pluripotency gene promoters - Bao, Xichen; Wu, Haitao; Zhu, Xihua; Guo, Xiangpeng; Hutchins, Andrew P; Luo, Zhiwei; Song, Hong; Chen, Yongqiang; Lai, Keyu; Yin, Menghui; Xu, Lingxiao; Zhou, Liang; et al. (Cell research, 2015)
Keywords: 631/337/176/1988; 631/337/384/2568; 631/532/2435; Animals; Apoptosis; Biomedical and Life Sciences; Cell Biology; Cell Proliferation; Cellular Reprogramming; CpG; CpG Islands; DNA (Cytosine-5-)-Methyltransferase 1; DNA (Cytosine-5-)-Methyltransferases - metabolism; DNA Methylation; Heterochromatin - genetics; Heterochromatin - metabolism; Histone-Lysine N-Methyltransferase - metabolism; Histones - genetics; Histones - metabolism; Induced Pluripotent Stem Cells - cytology; Induced Pluripotent Stem Cells - metabolism; Life Sciences; Methylation; Mice; Original; original-article; p53; Promoter Regions, Genetic; RNA, Long Noncoding - metabolism; Tumor Suppressor Protein p53 - metabolism; 体细胞; 全能性; 基因启动子; 基因诱导; 甲基化; 重编程; DNA methylation; long noncoding RNAs; somatic cell reprogramming; H3K9 methylation; p53; heterochromatin