Project description:Purpose: Endothelial cell-specific knockout of the INO80 chromatin-remodeling complex in developing mouse embryos results in defective coronary angiogenesis. Transcriptome analysis on whole hearts was performed to understand how Ino80 regulates the genome to influence angiogenesis. Methods: mRNA was extracted from whole hearts after surgical removal from embryonic day 13.5 mice, either WT or Tie2-Ino80 KO, and prepped for Illumina sequencing using the NEBNext Ultra RNA Library Prep kit. Results: Deletion of Ino80 in the two major coronary progenetiors results in intermediate non-compaction phenotypes and an increase in E2F-mediated gene expression and cellular proliferation. Conclusions: Ino80 normally functions to suppress E2F-mediated proliferation in cardiac endothelial cells in order to promote productive angiogenesis and prevent underdevelopment of the myocardium heart muscle. Loss of this critical chromatin-remodeling function results in human disease phenotypes.
Project description:Bulk RNA expression profiles were captured from hearts of alpha7 nicotinic acetylcholine receptor (Chrna7) knockout (KO) and wild type (WT) mice that underwent myocardial infarction (MI) or sham (SH) surgery at postnatal day 1 and full ventricle collection at 7 days post-surgery
Project description:Bulk RNA expression profiles were captured from hearts of Leucine-rich repeat containing protein 10 (Lrrc10) knockout (KO) and wild type (WT) mice that underwent myocardial infarction (MI) or sham (SH) surgery at postnatal day 1 and full ventricle collection at 7 days post-surgery
Project description:Transcriptional profiling of postpartum day 0 mouse brain, comparing TDAG51 wild-type (WT) vs TDAG51 knockout (KO), and TDAG51 KO transgenic (Tg) vs TDAG51 KO.
Project description:Using RNAseq to identify differentially expressed transcripts between CBFB wild type (WT) and knockout (KO) or between RUNX1 wild type (WT) and knockout (KO) MCF10A cells.
Project description:Immunoprecipitation of GNAQ protein by immunoprecipitation with two different antibodies from Santa Cruz Biotechnology (C-19 and E-17) in isolated mitochondria from different cell lines. The cell lines used include: Mouse embryonic fibroblasts (MEF) wild-type (WT), GNAQ knockout (KO) and knockout expressing GNAQ WT (KO_Gq). NIH3T3 cells were also used.
Project description:Metabolomics data from E. Coli Nissle (wild type, WT) and 3 E. Coli Nissle knockout (KO) strains grown in M-9 media and enriched M-9 media.
Project description:Slc39a8 KO mouse embryo hearts exhibit ventricle noncompaction phenotype which becomes evident at E12.5. The goal of this experiment is to identify genes that are differentially expressed between Slc39a8 KO and WT, which may be underlying the phenotype.
Project description:RhoE is a small GTPase that regulates actin cytoskeleton organization and cell migration. This analysis aimed at exploring the physiological function of RhoE in heart by means of knockout mouse model. We used microarrays to compare differentital gene expression profiles in wild-type and RhoE knockout embryo hearts.
Project description:To gain insight into the potential molecular mechanisms by which PGRN regulates influenza viral replication, proteomic analyses of whole mouse lung tissue from wild-type (WT) versus (vs) PGRN knockout (KO) mice were performed to identify proteins regulated by the absence vs presence of PGRN.
