Project description:This SuperSeries is composed of the following subset Series: GSE31171: Exon level expression profiling of mutant U2AF35 transduced HeLa cells GSE31172: Expression analysis of mutant U2AF35 transduced cells Refer to individual Series
Project description:In this study, to obtain the biological impact of the mutated U2AF35, HeLa cells were retrovirally transduced with either mock, wild-type or S34F mutant of U2AF35, and Exon array was performed. Exon level analysis was performed for mock, wild-type U2AF35 or S34F mutant transduced HeLa in triplicate.
Project description:In this study, to obtain the biological impact of the mutated U2AF35, HeLa cells were retrovirally transduced with either mock, wild-type or S34F mutant of U2AF35, and Exon array was performed.
Project description:In this study, to obtain the biological impact of the mutated U2AF35, HeLa and TF-1 cells were retrovirally transduced with either mock, wild-type or S34F mutant of U2AF35, and Expression array was performed. Expression analysis was performed for mock, wild-type U2AF35 or S34F mutant transduced HeLa and MDS-derived TF-1 cell line in triplicate.
Project description:In this study, to obtain the biological impact of the mutated U2AF35, HeLa and TF-1 cells were retrovirally transduced with either mock, wild-type or S34F mutant of U2AF35, and Expression array was performed.
Project description:The U2AF heterodimer has been well studied for its role in defining functional 3M-bM-^@M-^Y splice sites in pre-mRNA splicing, but many fundamental questions still remain unaddressed regarding the function of U2AF in mammalian genomes. Through genome-wide analysis of U2AF-RNA interactions, we report that U2AF has the capacity to directly define ~88% of functional 3M-bM-^@M-^Y splice sites in the human genome, but numerous U2AF binding events also occur in intronic locations. Mechanistic dissection reveals that upstream intronic binding events interfere with the immediate downstream 3M-bM-^@M-^Y splice site associated with either the alternative exon to cause exon skipping or with the competing constitutive exon to induce exon inclusion. We further demonstrate partial functional impairment with mutations in U2AF35, but not U2AF65, in regulated splicing. These findings reveal the genomic function and regulatory mechanism of U2AF in both normal and disease states. Examination of U2AF heterodimer regulated splicing in Hela cells with CLIP-seq (U2AF65), paired-end RNA-seq (si-NC and si-U2AF65) and RASL-seq (respective three biological replicates of WT, si-NC, si-U2AF65, si-U2AF35, si-NC + pcDNA3.0, si-U2AF65 + pcDNA3.0, and si-U2AF65 + Flag-U2AF35)
Project description:Exon Level Expression Profiling of HeLa cells depleted of DNMT1 by 2 independent siRNAs In HeLa cells where depletion of DNMT1 was sufficient to cause reduced levels of DNA methylation inside the body of CD44 and reduced usage of CD44 variant exons, without affecting splicing factors regulating CD44.
