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Cardiac cell type-specific gene regulatory programs and disease risk association [ATAC-seq]

ABSTRACT: Cardiac cell type-specific gene regulatory programs and disease risk association [ATAC-seq]

PROVIDER: PRJNA698273 | ENA |

REPOSITORIES: ENA

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Cardiac cell type-specific gene regulatory programs and disease risk association

Project description:Cardiac cell type-specific gene regulatory programs and disease risk association

| PRJNA698224 | ENA

Cardiac cell type-specific gene regulatory programs and disease risk association [RNA-seq]

Project description:Cardiac cell type-specific gene regulatory programs and disease risk association [RNA-seq]

| PRJNA698274 | ENA

Cardiac cell type-specific gene regulatory programs and disease risk association [ATAC-seq]

Project description:Misregulated gene expression in human hearts can result in cardiovascular diseases that are leading causes of morbidity and mortality worldwide. However, the limited information on the genomic location of candidate cis-regulatory elements (cCRE) such as enhancers and promoters in distinct cardiac cell types has restricted the understanding of these diseases. Here, we defined >287,000 cCREs in the four chambers of the human heart at single-cell resolution, which revealed cCREs and candidate transcription factors associated with cardiac cell types in a region-dependent manner and during heart failure. We further discovered cardiovascular disease-associated genetic variants enriched within these cCREs including 38 candidate causal atrial fibrillation variants localized to cardiomyocyte cCREs. Additional functional studies revealed that two of these variants affect a cCRE controlling KCNH2/HERG expression and action potential repolarization. Overall, this comprehensive atlas of human cardiac cCREs provides the foundation for illuminating cell type-specific gene regulation in human hearts during health and disease.

2021-04-01 | GSE165837 | GEO

Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs [ATAC-Seq]

Project description:Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs [ATAC-Seq]

| PRJNA771372 | ENA

Cardiac cell type-specific gene regulatory programs and disease risk association [RNA-seq]

2021-04-01 | GSE165838 | GEO

Genome-Wide Association Study of Lung Cancer Risk

Project description:Genome-Wide Association Study of Lung Cancer Risk

| PRJNA75801 | ENA

Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs

Project description:Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programs

| PRJNA771560 | ENA

ATAC-seq from cardiac septum (ENCSR167SYF)

Project description:ATAC-seq on human cardiac septum For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2022-10-16 | GSE215650 | GEO

Definition of germ cell lineage alternative splicing programs reveals a critical role for Quaking in specifying cardiac cell fate

Project description:Alternative splicing is critical for development. However, its role in the specification of the three embryonic germ layers is poorly understood. By performing RNA-Seq on human embryonic stem cells (hESCs) and derived endoderm, cardiac mesoderm, and ectoderm cell lineages, we detect distinct alternative splicing programs associated with each lineage. The most prominent splicing program differences are observed between definitive endoderm and cardiac mesoderm. Integrative multi-omics analyses link each program with lineage-specific RNA binding protein regulators, and further suggest a widespread role for Quaking (QKI) in the specification of cardiac mesoderm. Remarkably, knockout of QKI disrupts the cardiac mesoderm-associated alternative splicing program and formation of myocytes. These changes likely arise in part through reduced expression of BIN1 splice variants linked to cardiac development. Collectively, our results thus uncover alternative splicing programs associated with the three germ lineages and demonstrate an important role for QKI in the formation of cardiac mesoderm.

2022-02-01 | MSV000088762 | MassIVE

Cardiac cell type-specific gene regulatory programs and disease risk association

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

2021-04-01 | GSE165839 | GEO