Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell mRNA-sequencing reveals a regulatory network in Myh6-MCM;Ino80fl/fl heart with heart failure.

ABSTRACT: Among the multitude of genes that INO80 regulated, we sought to identify ones that acted more readily in response to INO80 overexpression, and whether those would form a regulatory network to execute a greater diversity of biological processes.

ORGANISM(S): Mus musculus

PROVIDER: GSE240181 | GEO | 2024/01/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

INO80 and heart failure.

Project description:INO80 and heart failure.

| PRJNA1002579 | ENA

Single-cell mRNA-sequencing reveals a regulatory network in Myh6-MCM Ino80fl/fl heart with heart failure.

Project description:Single-cell mRNA-sequencing reveals a regulatory network in Myh6-MCM Ino80fl/fl heart with heart failure.

| PRJNA1002583 | ENA

The distribution of INO80 in the development of heart failure.

Project description:We performed chromatin immunoprecipitation (ChIP) against the core subunit INO80 to determine its direct regulation on downstream targets.

2024-01-04 | GSE240179 | GEO

The effect of INO80 on chromatin accessibility in the development of heart failure.

Project description:In order to detect the effect of INO80 on chromatin accessibility, we will utilize the Assay for Transposase Accessible Chromatin with highthroughput sequencing (ATAC-Seq).

2024-01-04 | GSE240178 | GEO

Impact of MYH6 variants in hypoplastic left heart syndrome.

Project description:Hypoplastic left heart syndrome (HLHS) is a clinically and anatomically severe form of congenital heart disease (CHD). Although prior studies suggest that HLHS has a complex genetic inheritance, its etiology remains largely unknown. The goal of this study was to characterize a risk gene in HLHS and its effect on HLHS etiology and outcome. We performed next-generation sequencing on a multigenerational family with a high prevalence of CHD/HLHS, identifying a rare variant in the α-myosin heavy chain (MYH6) gene. A case-control study of 190 unrelated HLHS subjects was then performed and compared with the 1000 Genomes Project. Damaging MYH6 variants, including novel, missense, in-frame deletion, premature stop, de novo, and compound heterozygous variants, were significantly enriched in HLHS cases (P < 1 × 10-5). Clinical outcomes analysis showed reduced transplant-free survival in HLHS subjects with damaging MYH6 variants (P < 1 × 10-2). Transcriptome and protein expression analyses with cardiac tissue revealed differential expression of cardiac contractility genes, notably upregulation of the β-myosin heavy chain (MYH7) gene in subjects with MYH6 variants (P < 1 × 10-3). We subsequently used patient-specific induced pluripotent stem cells (iPSCs) to model HLHS in vitro. Early stages of in vitro cardiomyogenesis in iPSCs derived from two unrelated HLHS families mimicked the increased expression of MYH7 observed in vivo (P < 1 × 10-2), while revealing defective cardiomyogenic differentiation. Rare, damaging variants in MYH6 are enriched in HLHS, affect molecular expression of contractility genes, and are predictive of poor outcome. These findings indicate that the etiology of MYH6-associated HLHS can be informed using iPSCs and suggest utility in future clinical applications.

| S-EPMC5206387 | biostudies-literature

The distribution of INO80 in the development of heart failure.

Project description:The distribution of INO80 in the development of heart failure.

| PRJNA1002581 | ENA

The effect of INO80 on chromatin accessibility in the development of heart failure.

Project description:The effect of INO80 on chromatin accessibility in the development of heart failure.

| PRJNA1002582 | ENA

Whole-exome sequencing identifies R1279X of MYH6 gene to be associated with congenital heart disease.

Project description:BackgroundMyosin VI, encoded by MYH6, is expressed dominantly in human cardiac atria and plays consequential roles in cardiac muscle contraction and comprising the cardiac muscle thick filament. It has been reported that the mutations in the MYH6 gene associated with sinus venosus atrial septal defect (ASD type III), hypertrophic (HCM) and dilated (DCM) cardiomyopathies.MethodsTwo patients in an Iranian family have been identified who affected to Congenital Heart Disease (CHD). The male patient, besides CHD, shows that the thyroglossal sinus, refractive errors of the eye and mitral stenosis. The first symptoms emerged at the birth and diagnosis based on clinical features was made at about 5 years. The family had a history of ASD. For recognizing mutated gene (s), whole exome sequencing (WES) was performed for the male patient and variants were analyzed by autosomal dominant inheritance mode.ResultsEventually, by several filtering processes, a mutation in MYH6 gene (NM_002471.3), c.3835C > T; R1279X, was identified as the most likely disease-susceptibility variant and then confirmed by Sanger sequencing in the family. The mutation frequency was checked out in the local databases. This mutation results in the elimination of the 660 amino acids in the C-terminal of Myosin VI protein, including the vital parts of the coiled-coil structure of the tail domain.ConclusionsOur study represents the first case of Sinus venosus defect caused directly by MYH6 stop codon mutation. Our data indicate that by increase haploinsufficiency of myosin VI, c.3835C > T mutation with reduced penetrance could be associated with CHD.

| S-EPMC6029398 | biostudies-literature

Terminal heart failure

Project description:Rats overexpressing the human renin and angiotensinogen genes die after seven weeks of end organ damage. They develop hypertension, heart hypertrophy and proteinuria.We compared terminal heart failure, these are indeed terminally ill to double transgenic animals suffering on hypertension, proteinuria and heart hypertrophy. In addition, Losartan-treated animals (10 mg/kg/d)showed similar physiological parameters (normotension, no proteinuria and no heart hypertrophy compared to control sprague dawley rats. Keywords: other

2005-01-03 | GSE1557 | GEO

Acute heart failure facts and numbers: acute heart failure populations.

Project description:Acute heart failure (AHF) is a life-threatening emergency, which largely profits from early diagnosis and treatment. The prevalence of AHF is difficult to assess, estimates range between 1 and 12% in the general population. Despite recent therapeutic advances, in-hospital mortality is high with estimates varying from 4 and 18% in different registries. Due to large differences in AHF definitions and selection criteria AHF populations vary in their characteristics and outcomes. This is especially true for randomized clinical trials and the external validity of some of these trials is questionable. Additionally, the timing of data collection and/or initiation of new therapies vary with the setting of trials. The aim of this article is to call attention to the difference in AHF populations and to emphasize the need for research to clearly define these populations. AHF populations from registries and clinical trials are the basis for evidence-based management strategies. It is important that these populations represent the patients in whom these strategies will be applied in routine care.

| S-EPMC5074292 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data