Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MYOCD is required for cardiomyocytes induction from human urine cells and fibroblasts through remodeling chromatin

ABSTRACT: MYOCD is required for cardiomyocytes induction from human urine cells and fibroblasts through remodeling chromatin

PROVIDER: PRJNA741908 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14929742_1.fastq.gz	Fastqsanger.gz
	SRR14929742_2.fastq.gz	Fastqsanger.gz
	SRR14929743_1.fastq.gz	Fastqsanger.gz
	SRR14929743_2.fastq.gz	Fastqsanger.gz
	SRR14929744_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

MYOCD is required for cardiomyocytes induction from human urine cells and fibroblasts through remodeling chromatin [RNA-seq]

Project description:Despite direct reprogramming of human cardiac fibroblasts into induced cardiomyocytes (iCM) holds great potential for heart regeneration, the mechanisms are poorly understood. Whether other human somatic cells could be reprogrammed into cardiomyocytes is also unknown. Here, we report human urine cells (hUCs) could be efficiently converted into CM-like cells and the associated chromatin accessibility dynamics (CAD) by assay for transposase accessible chromatin(ATAC)-seq. hUCs transduced by MEF2C, TBX5, MESP1 and MYOCD but without GATA4 expressed multiple cardiac specific genes, exhibited Ca2+ oscillation potential and sarcomeric structures, and contracted synchronously in coculture with mouse CM. Additionally, we found that MYOCD is required for both closing and opening critical loci, mainly by hindering the opening of loci enriched with motifs for the TEAD and AP1 family and promoting the closing of loci enriched with ETS motifs. These changes differe partially from CAD observed during iCM induction from human fibroblasts. Collectively, our study offers one robust platform for iCM generation and insights into mechanisms for iCM fate determination.

2021-06-29 | GSE179012 | GEO

MYOCD is required for cardiomyocytes induction from human urine cells and fibroblasts through remodeling chromatin [ATAC-seq]

2021-06-29 | GSE179011 | GEO

MYOCD is required for cardiomyocytes induction from human urine cells and fibroblasts through remodeling chromatin [ATAC-seq]

Project description:MYOCD is required for cardiomyocytes induction from human urine cells and fibroblasts through remodeling chromatin [ATAC-seq]

| PRJNA741911 | ENA

MYOCD is required for cardiomyocytes induction from human urine cells and fibroblasts through remodeling chromatin [RNA-seq]

Project description:MYOCD is required for cardiomyocytes induction from human urine cells and fibroblasts through remodeling chromatin [RNA-seq]

| PRJNA741912 | ENA

RNA-Seq of Ctrl, Myocd KO, Mrtfa/b DKO and TKO cardiomyocytes

Project description:To characterize transcriptome changes uopn Myocd KO, Mrtfa/b DKO and Mrtfa/b/Myocd TKO in maturing cardiomyocytes

2022-08-01 | GSE210085 | GEO

MYOCD is required for cardiomyocytes induction from human urine cells and fibroblasts through remodeling chromatin

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

2021-06-29 | GSE179013 | GEO

RNA-Seq of Ctrl, Myocd KO, Mrtfa/b DKO and TKO cardiomyocytes

Project description:RNA-Seq of Ctrl, Myocd KO, Mrtfa/b DKO and TKO cardiomyocytes

| PRJNA863635 | ENA

MYOCD overexpression in HCASMs

Project description:To identify novel genes especially lncRNAs linked to vascular smooth muscle cell (VSMC) differentiation, we performed RNA sequencing of adenovirus–MYOCD transduced human coronary artery smooth muscle cells (HCASMs). Simiilar amount of empty Adenovirus was used as control.

2016-08-31 | GSE77120 | GEO

TFPa/HADHA is required for fatty acid beta-oxidation and cardiolipin re-modeling in human cardiomyocytes (part-I)

Project description:Mitochondrial trifunctional protein deficiency, due to mutations in hydratase subunit A (HADHA), results in sudden infant death syndrome (SIDS) with no cure. To reveal the disease etiology, we generated stem cell-derived cardiomyocytes from HADHA-deficient hiPSCs and accelerated their maturation via a novel, engineered MicroRNA Maturation Cocktail (MiMaC) that upregulated the epigenetic regulator, HOPX. Fatty acid challenged MiMaC treated HADHA mutant cardiomyocytes manifested the disease phenotype: defective calcium dynamics and repolarization kinetics which resulted in a pro-arrhythmic state. Single cell RNA-seq revealed a novel cardiomyocyte developmental intermediate, based on metabolic gene expression. This intermediate gave rise to mature-like cardiomyocytes in control cells but, mutant cells transitioned to a pathological state with reduced fatty acid beta-oxidation (FAO), reduced mitochondrial proton gradient, disrupted cristae structure and defective cardiolipin remodeling. This study reveals that TFPa/HADHA, a MLCL-AT-like enzyme, is required for FAO and cardiolipin remodeling, essential for functional mitochondria in human cardiomyocytes.

2019-08-26 | ST001246 | MetabolomicsWorkbench

Urine

Project description:Urine Raw sequence reads

| PRJNA850668 | ENA