Similar Datasets
Project description:The AE3 (Slc4a3) Cl/HCO3 exchanger is highly abundant in heart, but its function is not known. To assess its function we performed RNA Seq analysis of mRNA from hearts of AE3-null and wild-type mice. The patterns of differential gene expression indicate mild hypoxia, enhanced glucose metabolism, and reduced fatty acid metabolism in cardiac myocytes, which is consistent with the hypothesis that HCO3 extrusion by AE3 plays a role in carbon dioxide disposal.
2017-07-01 | GSE70471 | GEO
Project description:RNA-Seq analyses of Hv1 null hearts
| PRJNA802661 | ENA
Project description:As Grl/Hey2 directly binds DNA through E box motifs and mediates transcription repression, we aim to gain insights into potential target genes of Grl/Hey2 during heart regeneration. We performed RNA-seq analyses using total RNAs collected from 4-HT-treated Tg(cmlc2:creER;cmlc2:nRSGG) hearts and Tg(cmlc2:nRSGG) control hearts, as well as grl5nt-/- mutant hearts and wild-type hearts following ventricular resection at 7 dpa. Using RNA profile analyses, we have identified some potential genes act downstream of Grl/Hey2-dependent transcriptional repression during heart regeneration.
2020-09-14 | GSE129499 | GEO
Project description:This experiment aimed to investigate the transcriptional role of G4 resolvase Dhx36 in the adult mouse heart. We compared three pools of wild-type (WT) mouse hearts with three pools of Dhx36 conditional knockout (cKO) hearts. In the mutant mice, Dhx36 was conditionally deleted in cardiomyocytes using the Myh6-cre transgenic line. Each of the six pools was created using RNA extracted from 3-5 hearts from mice aged approximately 21 days. The cKO mice developed dilated cardiomyopathy and began experiencing sudden death at 40 days old, with no mutants surviving beyond 5 months.
2024-09-15 | E-MTAB-14440 | biostudies-arrayexpress
Project description:Mice lacking the zinc finger transcription factor Specificity protein 3 (Sp3) die prenatally in the C57Bl/6 background. To elucidate the cause of mortality we analyzed the potential role of Sp3 in embryonic heart development. Sp3 null hearts display defective looping at E10.5, and at E14.5 the Sp3 null mutants have developed a range of severe cardiac malformations. In an attempt to position Sp3 in the cardiac developmental hierarchy, we analysed the expression patterns of >15 marker genes in Sp3 null hearts. Expression of Cardiac ankyrin repeat protein (Carp) was downregulated prematurely after E12.5, while expression of the other marker genes was not affected. ChIP analysis revealed that Sp3 is bound to the Carp promoter region in vivo. Microarray analysis indicates that small molecule metabolism and cell-cell interactions are the most significantly affected biological processes in E12.5 Sp3 null myocardium. Since the epicardium showed distension from the myocardium, we studied expression of Wt1, a marker for epicardial cells. Wt1 expression was diminished in epicardium-derived cells in the myocardium of Sp3 null hearts. We conclude that Sp3 is required for normal cardiac development, and suggest that it has a crucial role in myocardial differentiation. ( Keywords: Transcription factors, Sp3, knockout mice, cardiac malformations, E12.5
2007-11-01 | GSE9124 | GEO
Project description:CCBE1 is a secreted extracellular matrix protein expressed by epicardial cells but its role during epicardial development was still unknown.Using a Ccbe1 knockout (KO) mouse model, we observed that loss of CCBE1 leads to congenital heart defects including thinner and hyper-trabeculated ventricular myocardium. In addition, Ccbe1 mutant hearts displayed reduced proliferation of cardiomyocyte and epicardial cells. RNA-seq data of CCBE1 KO and WT murine hearts indicated deregulation of genes associated with development and morphogenesis including the epithelial-to-mesenchymal transition.
2022-10-23 | E-MTAB-12217 | biostudies-arrayexpress
Project description:UnlabelledThe estimation of isoform abundances from RNA-Seq data requires a time-intensive step of mapping reads to either an assembled or previously annotated transcriptome, followed by an optimization procedure for deconvolution of multi-mapping reads. These procedures are essential for downstream analysis such as differential expression. In cases where it is desirable to adjust the underlying annotation, for example, on the discovery of novel isoforms or errors in existing annotations, current pipelines must be rerun from scratch. This makes it difficult to update abundance estimates after re-annotation, or to explore the effect of changes in the transcriptome on analyses. We present a novel efficient algorithm for updating abundance estimates from RNA-Seq experiments on re-annotation that does not require re-analysis of the entire dataset. Our approach is based on a fast partitioning algorithm for identifying transcripts whose abundances may depend on the added or deleted isoforms, and on a fast follow-up approach to re-estimating abundances for all transcripts. We demonstrate the effectiveness of our methods by showing how to synchronize RNA-Seq abundance estimates with the daily RefSeq incremental updates. Thus, we provide a practical approach to maintaining relevant databases of RNA-Seq derived abundance estimates even as annotations are being constantly revised.Availability and implementationOur methods are implemented in software called ReXpress and are freely available, together with source code, at http://bio.math.berkeley.edu/ReXpress/.Supplementary informationSupplementary data are available at Bioinformatics online.
| S-EPMC3694665 | biostudies-literature
Project description:A myofibroblast specific tamoxifen inducible Cre was used to assess the role of Yap and Wwtr1 in the mouse heart after myocardial infarction
2022-10-29 | GSE163612 | GEO
Project description:BackgroundHuntingtin (Htt) protein is the product of the gene mutated in Huntington's disease (HD), a fatal, autosomal dominant, neurodegenerative disorder. Normal Htt is essential for early embryogenesis and the development of the central nervous system. However, the role of Htt in adult tissues is less defined. Following the recent promising clinical trial in which both normal and mutant Htt mRNA were knocked down in HD patients, there is an urgent need to fully understand the molecular consequences of knocking out/down Htt in adult tissues. Htt has been identified as an important transcriptional regulator. Unbiased investigations of transcriptome changes with RNA-sequencing (RNA-Seq) have been done in multiple cell types in HD, further confirming that transcriptional dysregulation is a central pathogenic mechanism in HD. However, there is lack of direct understanding of the transcriptional regulation by normal Htt.MethodsTo investigate the transcriptional role of normal Htt, we first knocked out Htt in the human neuroblastoma SH-SY5Y cell line using the CRISPR (clustered regularly interspaced short palindromic repeats)-Cas9 (CRISPR-associated protein 9) gene editing approach. We then performed RNA-seq analysis on Htt-null and wild type SH-SY5Y cells to probe the global transcriptome changes induced by Htt deletion.ResultsIn general, Htt has a widespread effect on gene transcription. Functional analysis of the differentially expressed genes (DEGs) using various bioinformatic tools revealed irregularities in pathways related to cell communication and signaling, and more specifically those related to neuron development, neurotransmission and synaptic signaling. We further examined the transcription factors that may regulate these DEGs. Consistent with the disrupted pathways associated with cellular development, we showed that Htt-null cells exhibited slower cell proliferation than wild type cells. We finally validated some of the top DEGS with quantitative RT-PCR.ConclusionsThe widespread transcriptome changes in Htt-null cells could be directly caused by the loss of Htt-mediated transcriptional regulation or due to the secondary consequences of disruption in the gene regulatory network. Our study therefore provides valuable information about key genes associated with Htt-mediated transcription and improves our understanding of the molecular mechanisms underlying the cellular functions of normal and mutant Htt.
| S-EPMC8252266 | biostudies-literature
Project description:Total RNA was isolated from 3 WT and 3 ERRa null hearts and independent hybridizations were performed using MOE430 2.0 microarrays. Expression profiling was conducted to determine changes in gene expression in hearts lacking ERRa. The expression of genes involved in heart and muscle development, muscle contraction, lipid metabolism, OxPhos, protein metabolism and transcription were affected by the loss of ERRa. Keywords: microarray and genetic modification
2007-03-08 | GSE7196 | GEO