Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparison of gene expression pattern between wild-type and RhoE knockout embryo hearts

ABSTRACT: Comparison of gene expression pattern between wild-type and RhoE knockout embryo hearts

PROVIDER: PRJNA479470 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Comparison of gene expression pattern between wild-type and RhoE knockout embryo hearts

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.

2018-07-04 | GSE116594 | GEO

Comparison of gene expression pattern between Wild-type and Hypb knockout embryo yolk sacs

Project description:This study aimed at exploring the physiological function of mammalian HYPB by means of knockout mouse model. Homogenous disruption of mouse Hypb gene leads to embryonic lethality at E10.5-E11.5. Severe vascular defects were observed in the Hypb-/- embryos, yolk sac and placenta.In the mutant embryo and yolk sac, disorganized and abnormally dilated capillaries cannot be remodeled into large blood vessels or intricate networks. Thus, our results suggest that the mammalian HYPB HMT plays an important role in embryonic vascularization. Keywords: knockout, mouse embryo development, angiogenesis, yolk sac, E9.0, E10.5

2009-12-28 | GSE10113 | GEO

Caveolin-3 Knockout Hearts

Project description:Energy Substrate Uptake and Metabolism are Preserved in Hypertrophic Caveolin-3 Knockout Hearts Keywords: gene knockout

2009-03-04 | GSE10848 | GEO

Caveolin-1 Knockout Hearts

Project description:Hearts Lacking Caveolin-1 Develop Hypertrophy with Normal Cardiac Substrate Metabolism Keywords: gene knockout

2009-03-04 | GSE10849 | GEO

Comparison of gene expression data between control and tissue specific epicardial PDGF receptor (a and b) knockout embryonic hearts

Project description:Epicardial cells undergo an epithelial-to-mesenchymal transtion (EMT) to generate coronary vascular smooth muscle cells (VSMC) and cardiac fibroblasts. Little is known about the mechanisms regulating EMT or the in vivo signals directing epicardial-derived cell (EPDC) fate. Here, we show that loss of PDGF signaling leads to a disruption in Sox9 expression, and when Sox9 expression was restored in mutant hearts, the EMT defect was rescued. Interestingly, mutants lacking only one of the PDGF genes exhibited a lineage specific requirement for the individual receptors. Loss of PDGFRα resulted in a deficit in cardiac fibroblast formation, while cVSMC development was unperturbed. Conversely, PDGFRβ was required for cVSMC development but not cardiac fibroblast development. Combined, our data demonstrate a novel role for PDGF receptors in epicardial EMT and EPDC development. GSM671723-GSM671724: Total RNA was isolated from E12.5 control and PDGF receptor epicardial knockout hearts using the Trizol reagent. RNA was processed as per manufacturer's instructions (Illumina Gene expression array, Illumina, inc. San Diego, CA, USA) GSM671877-GSM671882: Total RNA was isolated from E12.5 control and PDGF receptor epicardial knockout primary epicardial cultures using the Trizol reagent. RNA was processed as per manufacturer's instructions (Illumina Gene expression array, Illumina, inc. San Diego, CA, USA)

2011-02-28 | E-GEOD-27181 | biostudies-arrayexpress

Wildtype vs. CENPF knockout heart comparison

Project description:We are comparing differential gene expression in WT vs. CENPF knockout hearts RNA was extracted from WT and CENPF knockout mouse hearts at 12 months and submitted to Vanderbilt Microarray core for processing

2012-02-01 | E-GEOD-35470 | biostudies-arrayexpress

RNA-sequencing from wild-type (WT) or Tie2-Ino80 knockout (KO) mouse embryo hearts

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.

2017-11-21 | GSE98082 | GEO

Transcription profiling of mouse caveolin-3 knockout hearts

Project description:Energy Substrate Uptake and Metabolism are Preserved in Hypertrophic Caveolin-3 Knockout Hearts Experiment Overall Design: 3 wild types, 3 knockouts

2009-03-15 | E-GEOD-10848 | biostudies-arrayexpress

Wildtype vs. CENPF knockout heart comparison

Project description:We are comparing differential gene expression in WT vs. CENPF knockout hearts

2012-02-01 | GSE35470 | GEO

Pattern of Islr knockout mouse colon gene expression

Project description:Pattern of Islr knockout mouse colon gene expression

| PRJNA558058 | ENA