Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cardiac gene expression profiling of Salvador mutant mice

ABSTRACT: In this study, we identified a number of genes whose expression are regulated by the Hippo tumor suppressor pathway. To disrupt Hippo signaling in the mouse heart, we inactivated the single mammalian Salv ortholog using a Salv conditional null allele and the Nkx2.5 cre allele that directs cardiac cre activity. Total RNA from embryonic hearts were used for expression profiling of 17,455 unique genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE27259 | GEO | 2011/02/12

SECONDARY ACCESSION(S): PRJNA137165

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Cardiac gene expression profiling of neonatal Salvador mutant mice

2015-05-12 | GSE44103 | GEO

Cardiac gene expression profiling of Salvador mutant mice

Project description:In this study, we identified a number of genes whose expression are regulated by the Hippo tumor suppressor pathway. To disrupt Hippo signaling in the mouse heart, we inactivated the single mammalian Salv ortholog using a Salv conditional null allele and the Nkx2.5 cre allele that directs cardiac cre activity. Total RNA from embryonic hearts were used for expression profiling of 17,455 unique genes. Genes transcriptionally regulated by the Hippo pathway during cardiogenesis were identifed through expression profiling of 17,455 unique genes in Salvador mutant (Salv CKO) embryonic hearts. Total RNA from E9.5-stage hearts were pooled into biological replicate samples (2 control and 2 Salv CKO) and were used to generate expression profiles.

2011-02-12 | E-GEOD-27259 | biostudies-arrayexpress

Cardiac gene expression profiling of neonatal Salvador mutant mice

Project description:In this study, we identified a number of genes whose expression are regulated by the Hippo tumor suppressor pathway. To disrupt Hippo signaling in the mouse heart, we inactivated the single mammalian Salv ortholog using a Salv conditional null allele and the Nkx2.5 cre allele that directs cardiac cre activity. Total RNA from P8-stage hearts were used for expression profiling. Genes transcriptionally regulated by the Hippo pathway during cardiogenesis were identifed through expression profiling in Salvador mutant (Salv CKO) neontate hearts. Total RNA from postnatal day 8 (P8)-stage hearts was purified to generate biological replicate samples (2 control and 2 Salv CKO) and generate expression profiles. 3 technical replicates were used for each sample.

2015-05-12 | E-GEOD-44103 | biostudies-arrayexpress

Cardiac profiling of Yap-bound chromatin in neonatal Salvador mutant mice

Project description:In this study, we identified chromatin regions bound by YAP, a major effector of the Hippo tumor suppressor pathway. To disrupt Hippo signaling in the mouse heart, we inactivated the single mammalian Salv ortholog using a Salv conditional null allele and and tamoxifen inducible Myh6-cre/Esr1 allele, Cre activity was induced with 4 consecutive intraperitoneal (i.p.) or subcutaneous injections of tamoxifen from P7-P10.

2019-09-25 | GSE46529 | GEO

Dicer conditional knockout embryonic heart mutant vs control array

Project description:The goal is to find out the gene expression changes when Dicer was inactivated in the murine heart. Keywords: Dicer mutant Dicer gene was specifically inactivated in the mouse heart using cardiac specific Nkx2.5 Cre knock-in line. Embryonic day 11.5 heart from mutant and control hearts were compared in triplicates.

2010-06-11 | E-GEOD-7343 | biostudies-arrayexpress

miR-302-367 regulates cardiomycyte proliferation and differentiation during development

Project description:To define the role of miR-302-367 cluster in cardiac development, we overexpressed miR-302-367 cluster in mouse heart by using R26R-miR-302-367; Nkx2.5-Cre mice. This data set contains the microarrays examining gene expression in the hearts of R26R-miR-302-367; Nkx2.5-Cre mice at postnatal day 14. We overexpressed miR-302-367 cluster in developing mouse heart using Nkx2.5-Cre mouse line

2015-01-01 | E-GEOD-54988 | biostudies-arrayexpress

miR-302-367 regulates cardiomycyte proliferation and differentiation during development

2015-01-01 | GSE54988 | GEO

Lats1/2 depletion in male sertoli cells

Project description:In order to understand the role of Hippo pathway in mice testes, we inactivated lats1/2 in a transgenic mouse model using the cre recombinase system in Sertoli cells. RNAseq analysis on whole e15.5 testes were performed on male mice

2024-04-22 | GSE243216 | GEO

Transcription profiling of mouse heart from cardiac-specific conditional knockout deletion of menage-a-trios-1 (MAT1)

Project description:The Cdk7/cyclin H/menage-a-trois 1 (MAT1) heterotrimer has proposed functions in transcription as the kinase component of basal transcription factor TFIIH and is activated in adult hearts by hypertrophic pathways. Using cardiac-specific Cre, we ablated MAT1 in myocardium. Despite reduced Cdk7 activity, MAT1-deficient hearts grew normally. However, fatal heart failure ensued at 6-8 weeks. By microarray profiling, quantitative RT-PCR, and Western blotting at 4 weeks, genes for energy metabolism were found to be suppressed selectively, including targets of peroxisome proliferator-activated receptor-gamma coactivator-1 (PGC-1). Cardiac metabolic defects were substantiated in isolated perfused hearts and isolated mitochondria. In culture, deleting MAT1 with Cre disrupted PGC-1 function: PGC-1Î± failed to activate PGC-1-responsive promoters and nuclear receptors, GAL4-PGC-1Î± was functionally defective, and PGC-1Î² likewise was deficient. PGC-1 was shown to interact with MAT1 and Cdk7, in co-precipitation assays. Thus, we demonstrate an unforeseen essential role for MAT1 in operation of the PGC-1 family of co-activators. Experiment Overall Design: MAT1F/F mice (Korsisaari et al., 2002) were bred with mice expressing Cre recombinase under the control of the cardiomyocyte-specific Î±-myosin heavy chain (Î±MHC) promoter (Gaussin et al., 2002a) and back-bred to MAT1F/F mice to generate the cardiac-specific knockout (Î±MHC-Cre+/0; MAT1F/F; CKO; Fig. 1A, B). Control mice were Î±MHC-Cre+/0; MAT1F/+ littermates, differing by the presence of one wild-type MAT1 allele, and excluding Cre-mediated toxicity as a basis for phenotypic disparity. Cardiac RNA samples were analyze at 2 or 4 weeks of age (N = 3-5 for each condition tested.

2009-04-23 | E-GEOD-6662 | biostudies-arrayexpress

RNA-seq on enriched cardiac fibroblasts from the hearts of Hif-1a conditional knockout or heterozygous mice

Project description:In this project we explore the role of the master hypoxia regulator, Hypoxia inducible factor-1alpha (Hif-1a), in governing cardiac fibroblast (CF) function in homeostasis. CF-specific Hif-1a conditional knockout (cKO) mice were generated by breeding Pdgfra-merCremer (PdgfraMCM/+) Cre recombinase driver mice with Hif-1a-floxed mice (Hif-1aflox/). In Hif-1afl/-; PdgfraMCM/+ progeny, Hif-1a could be conditionally deleted in adult CFs by tamoxifen (tam) administration. We also introduced a Cre-dependent R26tdTomato reporter allele allowing marking of Pdgfra+ CFs and their progeny. In this experiment, we performed bulk RNA sequencing (RNA-seq) on tdTomato+ cells from the hearts of healthy cKO or heterozygous (HET) adult, male mice.

2021-11-11 | E-MTAB-9674 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data