NUP155 insufficiency recalibrates a pluripotent transcriptome with network remodeling of a cardiogenic signaling module.

ABSTRACT:

Background

Atrial fibrillation is a cardiac disease driven by numerous idiopathic etiologies. NUP155 is a nuclear pore complex protein that has been identified as a clinical driver of atrial fibrillation, yet the precise mechanism is unknown. The present study employs a systems biology algorithm to identify effects of NUP155 disruption on cardiogenicity in a model of stem cell-derived differentiation.

Methods

Embryonic stem (ES) cell lines (n = 5) with truncated NUP155 were cultured in parallel with wild type (WT) ES cells (n = 5), and then harvested for RNAseq. Samples were run on an Illumina HiSeq 2000. Reads were analyzed using Strand NGS, Cytoscape, DAVID and Ingenuity Pathways Analysis to deconvolute the NUP155-disrupted transcriptome. Network topological analysis ident

SUBMITTER: Preston CC 

PROVIDER: S-EPMC5977756 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature