ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/009/ERR6221529/ERR6221529_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/003/ERR6221523/ERR6221523_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/008/ERR6221528/ERR6221528_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/007/ERR6221527/ERR6221527_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/002/ERR6221522/ERR6221522_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/006/ERR6221526/ERR6221526_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/009/ERR6221529/ERR6221529_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/000/ERR6221530/ERR6221530_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/004/ERR6221524/ERR6221524_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/003/ERR6221523/ERR6221523_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/000/ERR6221530/ERR6221530_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/008/ERR6221528/ERR6221528_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/006/ERR6221526/ERR6221526_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/005/ERR6221525/ERR6221525_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/007/ERR6221527/ERR6221527_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/004/ERR6221524/ERR6221524_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/002/ERR6221522/ERR6221522_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR622/005/ERR6221525/ERR6221525_1.fastq.gzprimaryOK200GenomicsEuropean Bioinformatics InstituteGehring Lab Institute for Genetics University of Colognehttps://www.ebi.ac.uk/ena/browser/view/PRJEB46200ArrayExpressUPF3A and UPF3B are paralogous genes in human cells that are involved in the nonsense-mediated decay (NMD) pathway. NMD is a cellular quality control mechanism that monitors mRNAs during translation. Aberrant translation due to features such as the presence of a premature stop codon downstream on an exon-exon junction activates NMD and leads to the degradation of the mRNA. To investigate the role of UPF3B and UPF3A in NMD, we have generated UPF3B knockout human Flp-In T-REx 293 cells using CRISPR-Cas9. We generated RNA-Sequencing data for wildtype and UPF3B KO cells with additional siRNA-mediated knockdown of Luciferase (Luc) as control or UPF3A.ENAfalseRNA-Seq of WT Flp-In T-REx 293 and UPF3B knockout cell lines with additional siRNA-mediated control or UPF3A knockdownsRNA-Seq of WT Flp-In T-REx 293 and UPF3B knockout cell lines with additional siRNA-mediated control or UPF3A knockdowns2022-04-262022-04-26PRJEB46200