Project description:To investigate the role of the lncRNA Charme in cardiac differentiation and physiology, total RNA was collected from CharmeWT and CharmeKO hearts RNA-seq analysis was performed on CharmeWT and CharmeKO postnatal hearts
Project description:MATR3 CLIP-seq analysis on embryonal (E15) murine hearts was performed to identify the protein RNA-interactors during murine cardiac development and to characterize the differential binding of the protein in conditon of KO of the lncRNA Charme.
Project description:We reported loss of HBL1 lncRNA promoted cardiogenesis. Here we wanted to know the genomewide gene expression profiles caused by HBL1 KO during cardiac differentiation.
Project description:The expression of the small molecular weight heat shock protein (Hsp) H11 kinase/Hsp22 (Hsp22) is restricted to a limited number of tissues, including the heart and skeletal muscle, both in rodents and in humans. We generated a mouse knockout (KO) model, and investigated the role of Hsp22 in regulating cardiac hypertrophy in response to pressure overload. We compared gene expression profiles between WT and KO mice in basal condition and three days pressure overload after transverse aortic constriction (TAC). These data illustrated a novel mechanism of Hsp22-related gene expression in response to cardiac stress. We used microarray to examine differential gene expression by Hsp22 deletion at baseline and 3-day pressure overload. Left ventricles from wild type and Hsp22 knockout mice were selected from basal condition (each, n=3) and TAC surgery (each, n=4).
Project description:Genome-wide transcriptomic analyses in left ventricles (LVs) from cardiac-specific miR-150 conditional knockout KO (cKO) mice were performed to identify novel miR-150 targets in the heart.
Project description:Analysis of different expression after lncRNA DHRS4-AS1 knockout with two strategies in immortalized human pancreatic duct epithelial cell line HPDE6-C7. The strategies include promoter-exon1 (PE) and branch point and 3‘ splicing site (BESST). The results provide transcriptome comparison between PE and BESST knockout approach, indicating the superior effect of BESST.
Project description:Analysis of different expression of mRNAs and lncRNAs after lncRNA DHRS4-AS1 knockout with two strategies in immortalized human pancreatic duct epithelial cell line HPDE6-C7. The strategies include promoter-exon1(PE) and branch point and 3‘ splicing site(BESST). The results provide transcriptome comparison between PE and BESST knockout approach, indicating the superior effect of BESST.
Project description:Previously, lncRNA Malat1 knockout mice were generated by insertional inactivation. By crossing this line to MMTV-PyMT mammary tumor mouse model, we produced PyMT;Malat1 wild-type (WT) and PyMT;Malat1 knockout (KO). Furthermore, we generated Malat1 transgenic mice by targeting ROSA26 locus and bred them to PyMT;Malat1 knockout mice to produce Malat1-rescued PyMT;Malat1 knockout;Malat1 transgenic animals (TG). Using mammary tumors from the three groups of animals, we performed RNA-Seq analysis to identify differentially up-regulated genes in KO tumors to find novel target genes of YAP-TEAD pathway.
Project description:Cardiac fibrosis occurs in most cardiac diseases, which reduces cardiac muscle compliance, impairs both systolic and diastolic heart function and, ultimately, leads to heart failure. Using unbiased transcriptome profiling in a mouse model of myocardial infarction, we identified a cardiac-fibroblast enriched lncRNA (AK048087) named cardiac fibroblast-associated transcript (Cfast), which is significantly elevated after myocardial infarction. Here, we show that silencing Cfast expression by lentiviral shRNAs resulted in suppression of fibrosis-related gene expression and transdifferentiation of myofibroblasts into cardiac fibroblasts. We performed the RNA-seq profiling in both lentivirus Cfast knockdown and lentivirus scramble group in cardiac fibroblasts. Finally, the transcriptome analysis indicates that genes related to cell differentiation, cell migration, extracellular matrix organization downregulated in Cfast knockdown group.