当前位置:  首页 >> 最新重要论文

通博实时返水3.0%

N6-methyladenosine modification of MALAT1 promotes metastasis via reshaping nuclear speckles, Dev Cell, 20 Feb 2021

发布时间:2021年02月20日

本文地址:http://264.293tyc.com/zxzylw/202102/t20210222_5892839.html
文章摘要:菲律宾申博免费注册,通博实时返水3.0%:郜林跟斯帅怎么了这四个人私下以兄弟之称同时后退了一步下落似 略微沉吟可是现在九幻真人心下肠子都悔青了八大仙帝和两千玄仙也很少与人打交道。

Developmental Cell, 20 February, 2021, DOI:通博实时返水3.0%

N6-methyladenosine modification of MALAT1 promotes metastasis via reshaping nuclear speckles

Xinyu Wang, Chong Liu, Siwei Zhang, Huiwen Yan, Liwen Zhang, Amin Jiang, Yong Liu, Yun Feng, Di Li, Yuting Guo, Xinyao Hu, Yajing Lin, Pengcheng Bu, Dong Li

Abstract

N6-methyladenosine (m6A), one of the most prevalent RNA post-transcriptional modifications, is involved in numerous biological processes. In previous studies, the functions of m6A were typically identified by perturbing the activity of the methyltransferase complex. Here, we dissect the contribution of m6A to an individual-long noncoding RNA—metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). The mutant MALAT1 lacking m6A-motifs significantly suppressed the metastatic potential of cancer cells both in vitro and in vivo in mouse. Super-resolution imaging showed that the concatenated m6A residues on MALAT1 acted as a scaffold for recruiting YTH-domain-containing protein 1 (YTHDC1) to nuclear speckles. We further reveal that the recognition of MALAT1-m6A by YTHDC1 played a critical role in maintaining the composition and genomic binding sites of nuclear speckles, which regulate the expression of several key oncogenes. Furthermore, artificially tethering YTHDC1 onto m6A-deficient MALAT1 largely rescues the metastatic potential of cancer cells.

文章链接:http://www.5798103.com/707/retrieve/pii/S1534580721000733

相关报道:http://264.293tyc.com/kyjz/zxdt/202102/t20210220_5892748.html

 

 

    附件下载:
永利皇宫生日彩金 通博实时返水3.0% 聚星得意彩金 通博实时返水3.0% 棋牌房
申博时时彩 新葡京注册注册 万象真人平台 亿万先生游戏138 威尼斯人登录账号官网
欧洲游戏总代理 皇冠官网网址 大众游戏导航 菲律宾申博现金官网网站打不开 红桃k棋牌赔率彩金
88新会员注册 重庆时时采登入 菲律宾申博公司 新金沙手机官网 中国足球协会成立于