Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing (eCLIP)

ABSTRACT: Homozygous R636S mutation was created by genome editing in an iPS cell line generated from a healthy female patient. Mutant and wild-type cells were differentiated into cardiomyocytes by modulating the WNT signaling pathway, and then are subjected to the lactate purification method. eCLIP was performed to identify targets of RBM20 in mutant and wild-type iPSC-CMs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE176060 | GEO | 2021/06/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing (WTB RNA-Seq)

Project description:RBM20 heterozygous (Het) mutation was created by genome editing in an iPS cell line generated from a healthy female patient. Those cells were differentiated into cardiomyocytes by modulating the WNT signaling pathway, and then are subjected to the lactate purification method.

2021-06-03 | GSE176045 | GEO

RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing [RNA-Seq]

Project description:RBM20 heterozygous (Het) and homozygous (Homo) R636S and homozygous 8-bp deletion (which causes nonsense-mediated decay) mutations were created by genome editing in an iPS cell line generated from a healthy male patient. Those cells were differentiated into cardiomyocytes by modulating the WNT signaling pathway, and then are subjected to the lactate purification method.

2019-05-02 | GSE113947 | GEO

RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing (RiboMinus RNA-Seq)

2021-06-01 | GSE175885 | GEO

Mislocalization of pathogenic RBM20 variants in dilated cardiomyopathy is caused by loss-of-interaction with Transportin-3

Project description:First, we compared gene expression and alternative splicing changes between differentially-localized P633L-RBM20, WT-RBM20, and R634Q-RBM20 in iPSC-CMs. Using ICS, we sorted iPSC-CMs with differentially-localized RBM20 based on correlation with nuclear staining. This was followed by RNA-sequencing of the sorted populations. Second, we analysed gene expression and splicing changes in iPSC-CMs overexpressing of WT-, R634Q-, or NLS-tagged R634Q-RBM20 in splice deficient cells carrying the homozygous frameshift mutation (S635FS). Third, we performed RNA sequencing of our HeLa Tet:Cas9 eGFP-RBM20-WT and -R634Q to compare their gene expression to iPSC-CMs. Lastly, we performed two genome-wide CRISPR ICS screens in HeLa cells stably expressing eGFP-RBM20-WT and -R634Q, and TetO-Cas9, to identify genes essential for RBM20 nuclear import.

2023-06-19 | GSE220833 | GEO

RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-01 | GSE175886 | GEO

RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing

Project description:RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing

| PRJNA734252 | ENA

RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing (eCLIP)

Project description:RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing (eCLIP)

| PRJNA734705 | ENA

RBM20 orchestrates cardiac pre-mRNA

Project description:The RNA-binding protein RBM20 has been implicated in dilated cardiomyopathy (DCM), a major cause of chronic heart failure. To determine how RBM20 regulates alternative splicing, we combined transcriptome-wide CLIP-seq, RNA-seq, and quantitative proteomics in cell culture, rat, and human hearts. Our analyses revealed a distinct RBM20 RNA-recognition element in predominantly intronic binding sites and linked repression of exon splicing with RBM20-binding near 3prime- and 5prime-splice sites. Our proteomic data show RBM20 interaction with U1- and U2-snRNPs and suggests splicing repression through spliceosome stalling at complex A. Among direct RBM20 targets are several genes involved in DCM as well as new genes not previously associated with the disease process. In human failing hearts, we demonstrate that reduced expression levels of RBM20 affect alternative splicing of several direct targets, indicating that differences in RBM20 gene expression may affect cardiac function. These findings reveal a new mechanism to understand the pathogenesis of human heart failure. The provided data files for RNA-seq contain information for reads that map to human RBM20 only.

2014-11-11 | E-MTAB-2572 | biostudies-arrayexpress

RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing [RNA-Seq]

Project description:RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing [RNA-Seq]

| PRJNA454577 | ENA

RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing (WTB RNA-Seq)

Project description:RNA-Seq of isogenic human iPS cell-derived cardiomyocytes with RBM20 mutations created by genome editing (WTB RNA-Seq)

| PRJNA734628 | ENA