Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

FHL5 cofactor mediates vascular disease risk by regulating smooth muscle cell transcriptional networks

ABSTRACT: FHL5 cofactor mediates vascular disease risk by regulating smooth muscle cell transcriptional networks

PROVIDER: PRJNA832245 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18923422_1.fastq.gz	Fastqsanger.gz
	SRR18923422_2.fastq.gz	Fastqsanger.gz
	SRR18923423_1.fastq.gz	Fastqsanger.gz
	SRR18923423_2.fastq.gz	Fastqsanger.gz
	SRR18923424_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 34

Similar Datasets

FHL5 cofactor mediates vascular disease risk by regulating smooth muscle cell transcriptional networks [RNA-seq]

Project description:FHL5 cofactor mediates vascular disease risk by regulating smooth muscle cell transcriptional networks [RNA-seq]

| PRJNA832251 | ENA

FHL5 cofactor mediates vascular disease risk by regulating smooth muscle cell transcriptional networks [CUT&RUN]

Project description:FHL5 cofactor mediates vascular disease risk by regulating smooth muscle cell transcriptional networks [CUT&RUN]

| PRJNA832252 | ENA

FHL5 cofactor mediates vascular disease risk by regulating smooth muscle cell transcriptional networks [RNA-seq]

Project description:Genome-wide association studies (GWAS) have identified hundreds of loci associated with vascular diseases such as coronary artery disease (CAD) and myocardial infarction (MI), and hypertension. However, the biological roles for many of these loci enriched in the vessel wall remains unknown. Among these, UFL1-FHL5 (chr6q16.1) emerged as a genome-wide significant locus in a recent CAD/MI meta-analysis. Here, we use an integrative approach leveraging human genetics, epigenomic profiling, and in vitro functional and ex vivo imaging analyses to prioritize FHL5 as the top candidate causal gene and reveal the molecular mechanisms of its pleiotropic genetic associations. Notably, FHL5 overexpression in coronary artery smooth muscle cells (SMC) increased vascular calcification and dysregulated processes related to extracellular matrix organization and calcium handling. Lastly, by mapping FHL5 binding sites genome-wide using CUT&RUN, we identified regulatory interactions with downstream disease loci having putative roles in SMC phenotypic modulation. Together, these trans-acting mechanisms may account for a portion of the heritable risk for CAD/MI and other complex vascular diseases.

2022-10-31 | GSE201571 | GEO

FHL5 cofactor mediates vascular disease risk by regulating smooth muscle cell transcriptional networks [CUT&RUN]

2022-10-31 | GSE201570 | GEO

FHL5 cofactor mediates vascular disease risk by regulating smooth muscle cell transcriptional networks

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

2022-10-31 | GSE201572 | GEO

Heterogeneous Expression of Alternatively Spliced lncRNA mediates Vascular Smooth Cell Plasticity

Project description:Heterogeneous Expression of Alternatively Spliced lncRNA mediates Vascular Smooth Cell Plasticity

| PRJNA869091 | ENA

LncVSM (AK098656) down-regulation in Vascular Smooth Muscle cells

Project description:The full length of LncVSM transfected into Vascular Smooth Muscle cells to down-regulation for screening differential expression prolifes of LncVSM effecting.The empty vector transfected Vascular Smooth Muscle cells as controls. Eight Samples analyzed.

2016-01-12 | E-GEOD-76720 | biostudies-arrayexpress

YAP/TAZ in vascular smooth muscle

Project description:YAP/TAZ in vascular smooth muscle

| PRJNA610067 | ENA

Rat vascular smooth muscle cells LC-MS/MS

Project description:Crotonylation of histones is discovered of late as one of post-translational modification that can regulate gene expression. However, the function of crotonylation on non-histone proteins in vascular smooth muscle cells (VSMC) is unclear. Here, we aim to use modification and proteomic analysis to find the cellular characteristic of crotonylated non-histone proteins and the crosstalk with ubiquitinated proteins in vascular smooth muscle cell (VSMC) phenotypic remodeling. We performed modification and proteomic analysis of VSMCs before and after stimulated with platelet-derived growth factor-BB (PDGF-BB). The crotonylated and ubiquitinated pan-antibody was used to enrich the protein and then subjected to high-throughput mass spectrometry analysis. The enrichment analysis was performed within differentially modified proteins in regards to GO terms, KEGG and protein domain.

2022-05-19 | PXD029070 | Pride

YAP/TAZ in vascular smooth muscle

Project description:Investigation of the physiogical functions of YAP/TAZ in vascular smooth muscle cells

2020-11-16 | GSE146317 | GEO