共查询到20条相似文献,搜索用时 46 毫秒
1.
2.
3.
4.
5.
6.
Gautier Koscielny Vincent Le Texier Chellappa Gopalakrishnan Vasudev Kumanduri Jean-Jack Riethoven Francesco Nardone Eleanor Stanley Christine Fallsehr Oliver Hofmann Meelis Kull Eoghan Harrington Stéphanie Boué Eduardo Eyras Mireya Plass Fabrice Lopez William Ritchie Virginie Moucadel Takeshi Ara Heike Pospisil Alexander Herrmann Daniel Gautheret 《Genomics》2009,93(3):213-220
7.
8.
Jihae Shin Qingbao Ding Luyang Wang Yange Cui Erdene Baljinnyam Aysegul Guvenek Bin Tian 《Nucleic acids research》2022,50(5):e25
Most human protein-coding genes produce alternative polyadenylation (APA) isoforms that differ in 3′ UTR size or, when coupled with splicing, have variable coding sequences. APA is an important layer of gene expression program critical for defining cell identity. Here, by using a catalytically dead Cas9 and coupling its target site with polyadenylation site (PAS), we develop a method, named CRISPRpas, to alter APA isoform abundance. CRISPRpas functions by enhancing proximal PAS usage, whose efficiency is influenced by several factors, including targeting strand of DNA, distance between PAS and target sequence and strength of the PAS. For intronic polyadenylation (IPA), splicing features, such as strengths of 5′ splice site and 3′ splice site, also affect CRISPRpas efficiency. We show modulation of APA of multiple endogenous genes, including IPA of PCF11, a master regulator of APA and gene expression. In sum, CRISPRpas offers a programmable tool for APA regulation that impacts gene expression. 相似文献
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
Venables JP 《BioEssays : news and reviews in molecular, cellular and developmental biology》2006,28(4):378-386
Alternative pre-mRNA splicing leads to distinct products of gene expression in development and disease. Antagonistic splice variants of genes involved in differentiation, apoptosis, invasion and metastasis often exist in a delicate equilibrium that is found to be perturbed in tumours. In several recent examples, splice variants that are overexpressed in cancer are expressed as hyper-oncogenic proteins, which often correlate with poor prognosis, thus suggesting improved diagnosis and follow up treatment. Global gene expression technologies are just beginning to decipher the interplay between alternatively spliced isoforms and protein-splicing factors that will lead to identification of the mutations in these trans-acting factors responsible for pathogenic alternative splicing in cancer. 相似文献