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Effect of cardiomyocyte KLF5 deletion in cardiac gene expression profile

ABSTRACT: Kruppel-like factor 5 gene was deleted (Cre-lox) system specifically in cardiomyocytes (aMHC-promoter-driven expression of Cre) and RNA was purified from total hearts (TRIZOL method) following perfusion of the heart with PBS. Basal levels cardiac RNA was analyzed with whole genome microarray chips.

ORGANISM(S): Mus musculus

PROVIDER: GSE63839 | GEO | 2014/12/05

SECONDARY ACCESSION(S): PRJNA269245

REPOSITORIES: GEO

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Effect of cardiomyocyte KLF5 deletion in cardiac gene expression profile

Project description:Kruppel-like factor 5 gene was deleted (Cre-lox) system specifically in cardiomyocytes (aMHC-promoter-driven expression of Cre) and RNA was purified from total hearts (TRIZOL method) following perfusion of the heart with PBS. Basal levels cardiac RNA was analyzed with whole genome microarray chips. There were two groups of mice: 4 mice that had KLF5 gene floxed without expressing Cre recombinase (control group) and 4 mice that were expressing Cre in cardiomyocytes and therefore KLF5 gene was deleted and thus not expressed in this particular cell type.

2014-12-05 | E-GEOD-63839 | biostudies-arrayexpress

Induction of adult cardiomyocyte renewal by Klf1

Project description:In highly regenerative animals, cardiac regeneration occurs innately through cardiomyocyte dedifferentiation and proliferation, although the regenerative mechanisms remain unclear. This project contains processed data sets that were used to identify that klf1, a Kruppel-like transcription factor essential for red blood cell development, is also necessary and sufficient in the myocardium for the induction of cardiomyocyte dedifferentiation and proliferation in adult zebrafish hearts. Raw data has been deposited to PRJNA551130

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Next Generation Sequencing of Wild-Type FVB/NJ Mouse Primary Cardiomyocyte and Cardiac Fibroblast Polyadenylated RNA and small RNA

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Gene Expression Following Transaortic Constriction in Cardiomyocyte Specific Insulin Receptor Substrate Knockout Mice

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Expression analysis of genes regulated by RBPJ (Notch) and Axin2 (Wnt) mediated signaling in mouse cardiogenesis at E9.25

Project description:Progenitor cells of the first and second heart fields (FHF and SHF) depend on cardiac-specific transcription factors for their differentiation. In mouse mutant embryos, we define the hierarchy of signaling events that controls the expression of cardiac-specific transcription factors during commitment of SHF progenitors at E9.25. Wnt and Bmp act downstream of Notch/RBPJ at this developmental stage. Mutation of Axin2, the negative regulator of canonical Wnt signaling, enhances Wnt and Bmp signals and suffices to rescue the cardiac differentiation arrest caused by loss of RBPJ. By analysis of isolated cardiac progenitors, embryo cultures in the presence of pharmacological inhibitors, and Bmp triple mutants, we could classify the expression of heart-specific transcription factors of SHF progenitors according to their dependence on either Wnt or Bmp signals, Nkx2-5, Isl1, Baf60c and Gata4, SRF, Mef2c, respectively. Total RNA from whole embryonic hearts of control mice was compared to MesP1-cre:RBPJlox/lox (KO), MesP1-cre:RBPJlox/lox//Axin2-/- (DKO), MesP1-cre:RBPJlox/+//Axin2-/- (hetDKO) and MesP1-cre:RBPJlox/lox//Axin2+/- (DKOhet) mutant mouse embryos.

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2020-11-01 | GSE106442 | GEO

SKP2 knockout in Rb1/p53 deficient transgenic mouse models of osteosarcoma induces macrophage infiltration and drives transcription of genes with favorable prognosis in patients

Project description:To study SKP2 in osteosarcoma, we generated a Skp2 KO line and a Skp2 intact line of transgenic OS mouse models: germline Skp2 knockout (“TKO”: Osx1-Cre;Rb1lox/lox;p53lox/lox;SKP2) versus Skp2 intact (“DKO”: Osx1-Cre;Rb1lox/lox;p53lox/lox). We then performed bulk RNAseq of the SKP2 KO vs SKP2 intact OS.

2023-10-02 | GSE226634 | GEO

Microarray analysis of gene expression in Rabgef1-knockout and control mouse skin

Project description:RABGEF1, a guanine nucleotide exchange factor for Rab5 GTPase, can negatively regulate mast cell activation in vitro. In addition, RabGEF1-deficient mice develop morbidity and severe skin inflammation associated with marked increases in skin mast cell numbers (Tam et al., Nat Immunol, 5(8):844-52, 2004). These findings suggest that over-reactive skin mast cells may contribute to the observed skin pathology in vivo. In order to identify the cell type(s) which contribute to skin inflammation when RabGEF1 is absent, we attempted to delete Rabgef1 gene specifically in three major skin cell types, namely mast cells, myeloid cells and keratinocytes; thus, Rabgef1 floxed (fl/fl) mice were crossed with mice expressing the Cre-recombinase under the influence of the promoter of Mcpt5, LysZ or K14, respectively. Unexpectedly, Mcpt5-Cre;Rabgef1fl/fl and Lysz-Cre;Rabgef1fl/fl mice appeared normal without phenotypic abnormalities. However, K14-Cre;Rabgef1fl/fl mice were normal at birth but rapidly developed morbidity and skin inflammation after 2-3 days, and died between 1 and 8 weeks of age. Skin (epidermis + dermis) was sampled from the center of the back behind shoulders, for 2 conditional knock-out mice (Rabgef1 lox/lox K14-Cre, hereafter called Rabgef1K-KO) and 2 control mice (Rabgef1 lox/lox). Total RNA was isolated from mouse skin using Trizol. Gene expression analysis was performed using Affymetrix Mouse Genome 430 2.0 arrays, with two replicates per genotype. Microarray data were analysed using Bioconductor for R.

2016-10-04 | E-MTAB-5000 | biostudies-arrayexpress

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