E-MTAB-10718
RNA-Seq of WT Flp-In T-REx 293, UPF3A knockout and UPF3A overexpression cell lines in part with additional siRNA-mediated control or UPF3B knockdowns
UPF3A 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 UPF3A knockout (KO)  human Flp-In T-REx 293 cells using CRISPR-Cas9, as well as FLAG-tagged UPF3A overexpressing cells using the PiggyBac transposon system. We generated RNA-Sequencing data for wildtype, UPF3A KO and UPF3A overexpressing (OE) cells, in part with additional siRNA-mediated knockdown of Luciferase (Luc) as control or UPF3B.
UPF3A 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 UPF3A knockout (KO)  human Flp-In T-REx 293 cells using CRISPR-Cas9, as well as FLAG-tagged UPF3A overexpressing cells using the PiggyBac transposon system. We generated RNA-Sequencing data for wildtype, UPF3A KO and UPF3A overexpressing (OE) cells, in part with additional siRNA-mediated knockdown of Luciferase (Luc) as control or UPF3B.