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Prolyl hydroxylation regulates protein degradation, synthesis, and splicing in human induced pluripotent stem cell-derived cardiomyocytes

ABSTRACT: In this study we report the gene expression profile and MISO analysis for alternative splicing events such as exon skipping in iPSC-derived cardiomyocytes which were treated with a drug inhibiting α-ketoglutarate-dependent hydroxylases (dimethyloxalylglycine) and compared to vehicle control. α-ketoglutarate-dependent hydroxylase inhibition plays a central role in cardiac hypoxia and the goal of this study was to identify new pathways in hypoxia beyond HIF-1α.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71560 | GEO | 2016/05/05

SECONDARY ACCESSION(S): PRJNA291518

REPOSITORIES: GEO

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The ribosomal prolyl-hydroxylase OGFOD1 decreases during cardiac differentiation, modulates translation and spliceosomal processes

Project description: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 α-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.

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Prolyl hydroxylation regulates protein degradation, synthesis and splicing in human induced pluripotent stem cell-derived cardiomyocytes

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Tuning the transcriptional response to hypoxia through HIF prolyl- and asparaginyl-hydroxylase inhibition:Sequencing Data

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Tuning the transcriptional response to hypoxia through HIF prolyl- and asparaginyl-hydroxylase inhibition: Microarray data

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