GSE130521
The ribosomal prolyl-hydroxylase OGFOD1 decreases during cardiac differentiation, modulates translation and spliceosomal processes
In this study we provide the gene expression profiles and MISO analyses for alternative splicing events such as exon skipping in wildtype versus OGFOD1 (oxoglutarate, glucose and iron dependent protein 1)-knock-out iPSC-derived cardiomyocytes, we further compare the profiles to wildtype which were treated with a drug  inhibiting a-ketoglutarate-dependent hydroxylases (dimethyloxalylglycine) versus vehicle control. Altered translation and splicing processes play a role in differentiation processes and have been shown to be involved in disease progression in e.g. heart failure. OGFOD1 is a ribosomal prolyl-hydroxylase and which influences translation, here we show its further importance in cardiac differentiation and alternative splicing. Overall design: Biological replicates of RNA-seq data from wildtype versus OGFOD1 (oxoglutarate, glucose and iron dependent protein 1)-knock-out iPSC-derived cardiomyocytes; wildtype treated with dimethyloxalylglycine or vehicle control