Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA282965 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hepatocyte-specific deletion of DNA methyltransferases Dnmt3a and Dnmt3b in mice
| PRJNA902086 | ENA
Project description:Cardiomyocyte-specific double knockout (DKO) mice lacking the catalytic domains of Dnmt3a (exon 18) and Dnmt3b (exon 19) were obtained by mating Dnmt3aflox and Dnmt3bflox mice [PMID 15757890] with mice expressing a cre recombinase under control of the cardiac atrial myosin light chain promoter (Myl7) [11689889]. Mice with the genotype Dnmt3aflox/flox, Dnmt3bflox/flox without expressing cre recombinase were used as control mice (CTL). Transcriptome analyses identified upregulation of 44 and downregulation of 9 genes in DKO as compared with control sham mice. TAC mice showed similar changes with substantial overlap of regulated genes compared to sham. Cardiac tissue from sham CTL (n=4) and DKO mice (n=4) as well as TAC-operated CTL (n=6) and DKO mice (n=6) was analysed.
2015-06-30 | E-GEOD-68518 | biostudies-arrayexpress
Project description:Cardiomyocyte-specific double knockout (DKO) mice lacking the catalytic domains of Dnmt3a (exon 18) and Dnmt3b (exon 19) were obtained by mating Dnmt3aflox and Dnmt3bflox mice [PMID 15757890] with mice expressing a cre recombinase under control of the cardiac atrial myosin light chain promoter (Myl7) [11689889]. Mice with the genotype Dnmt3aflox/flox, Dnmt3bflox/flox without expressing cre recombinase were used as control mice (CTL). Transcriptome analyses identified upregulation of 44 and downregulation of 9 genes in DKO as compared with control sham mice. TAC mice showed similar changes with substantial overlap of regulated genes compared to sham.
2015-06-30 | GSE68518 | GEO
Project description:Cytosine methylation is an epigenetic mark that dictates cell fate and response to stimuli. The timing and establishment of methylation logic during kidney development remains unknown. DNA methyltransferase 3a and 3b are the enzymes capable of establishing de novo methylation. We generated mice with genetic deletion of Dnmt3a and Dnmt3b in nephron progenitor cells (Six2Cre Dnmt3a/3b) and kidney tubule cells (KspCre Dnmt3a/3b). We characterized KspCre Dnmt3a/3b mice at baseline and after injury. Unbiased omics profiling, such as whole genome bisulfite sequencing, reduced representation bisulfite sequencing and RNA sequencing were performed on whole-kidney samples and isolated renal tubule cells. KspCre Dnmt3a/3b mice showed no obvious morphologic and functional alterations at baseline. Knockout animals exhibited increased resistance to cisplatin-induced kidney injury, but not to folic acid–induced fibrosis. Whole-genome bisulfite sequencing indicated that Dnmt3a and Dnmt3b play an important role in methylation of gene regulatory regions that act as fetal-specific enhancers in the developing kidney but are decommissioned in the mature kidney. Loss of Dnmt3a and Dnmt3b resulted in failure to silence developmental genes. We also found that fetal-enhancer regions methylated by Dnmt3a and Dnmt3b were enriched for kidney disease genetic risk loci. Methylation patterns of kidneys from patients with CKD showed defects similar to those in mice with Dnmt3a and Dnmt3b deletion. Our results indicate a potential locus-specific convergence of genetic, epigenetic, and developmental elements in kidney disease development.
2020-03-03 | GSE134267 | GEO
Project description:Genome-wide analysis of gene expression in the paraventricular nucleus of Sim1-Cre specific DNMT3a deletion mice.
| PRJNA181002 | ENA
Project description:Effect of cardiomyocyte KLF5 deletion in cardiac gene expression profile
| PRJNA269245 | ENA
Project description:<p>BACKGROUND: Imbalances in cardiac branched-chain amino acid (BCAA) metabolism and mitochondrial homeostasis are implicated in the onset and development of heart failure. However, the mechanisms triggering the downregulation of cardiac BCAA metabolism in heart failure remain unclear. Here, we identify a novel role of RNA-binding protein GRSF1 (guanine-rich RNA sequence binding factor 1) in post-transcriptionally regulating cell-intrinsic BCAA metabolic pathways, ultimately contributing to the pathogenesis of heart failure.</p><p>METHODS: We examined GRSF1 expression in the heart tissues of patients with dilated cardiomyopathy and generated mice with cardiomyocyte-specific deletion or overexpression of GRSF1 in vivo to investigate its role in heart failure. The effect of GRSF1 on BCAA homeostasis was assessed through untargeted and targeted metabolomics and mitochondrial function analysis. To elucidate the mechanisms underlying GRSF1-mediated metabolic regulation, we employed mice with cardiomyocyte-specific deletion of BCKDHB, and mice with cardiomyocyte-specific expression of GRSF1 lacking a quasi-RNA recognition motif. </p><p>RESULTS: GRSF1 expression was significantly decreased in the hearts of patients with heart failure and failing murine hearts. Cardiomyocyte-specific GRSF1 deletion resulted in cardiac dysfunction, spontaneous progression to dilated cardiomyopathy, and heart failure, accompanied by increased cardiac hypertrophy and fibrosis. Conversely, GRSF1 overexpression attenuated cardiac remodeling and heart failure induced by transverse aortic constriction. Mechanistically, GRSF1 maintained BCAA homeostasis and mitochondrial function by directly interacting with the G-tracts in coding region of BCKDHB mRNA through a quasi-RNA recognition motif to promote the stability of BCKDHB mRNA at the post-transcriptional level, thereby increasing its protein expression. Functional recovery mediated by GRSF1 overexpression in cardiomyocytes was partially blocked upon cardiac-specific deletion of BCKDHB. </p><p>CONCLUSIONS: Our study identified GRSF1 as a cell-intrinsic metabolic checkpoint that maintains cardiac BCAA homeostasis by regulating BCKDHB mRNA turnover. Targeting GRSF1 may offer therapeutic benefits for heart failure and other cardiometabolic diseases requiring BCAA manipulation.</p>
2025-10-19 | MTBLS13178 | MetaboLights
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Hearts were taken from wide type and Myc-null Mouse embryos at E13.5 under the dissecting scope. Cardiac myocyte RNA was isolated using TRIZOL®Reagent Total RNA (100 ng) was hybridized to the Sentrix® MouseRef-8 Expression BeadChip that contains probes for ~24,000 transcripts. GeneChips were scanned using the Hewlett-Packard GeneArray Scanner G2500A. The data were analyzed with Illumina Inc. BeadStudio version 1.5.0.34 and normalized by rank invariant method.
2010-06-10 | E-GEOD-7162 | biostudies-arrayexpress
Project description:Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development
| PRJNA356839 | ENA
Project description:Cardiomyocyte-specific FGFR1 knockout attenuates Ang II-induced cardiac remodeling
| PRJNA1001173 | ENA