Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-GEOD-6662

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

OTHER RELATED OMICS DATASETS IN: PRJNA98623

PROVIDER: E-GEOD-6662 | ExpressionAtlas | 2014-10-10

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-GEOD-6662-analysis-methods.tsv	Tabular
	E-GEOD-6662-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-6662-configuration.xml	Xml
	E-GEOD-6662-percentile-ranks.tsv	Tabular
	E-GEOD-6662.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 70

Similar Datasets

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

E-GEOD-58719

Project description:Expression data from conditional Klf5 knockout Pten-null mouse prostates

2015-08-04 | E-GEOD-58719 | ExpressionAtlas

E-GEOD-11759

Project description:Transcription profiling of mouse conditional intestinal epithelial Hnf4Ialpha knockout to investigate the role of HNF4alpha in the adult colon

2015-01-13 | E-GEOD-11759 | ExpressionAtlas

E-GEOD-48622

Project description:Transcriptional Profiling of Neuronal APP/APLP2 Double-Conditional Knockout Mice.

2015-07-16 | E-GEOD-48622 | ExpressionAtlas

Cardiac-specific deletion of ménage-à-trois-1 (MAT1)

Project description:The Cdk7/cyclin H/ménage-à-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-1α failed to activate PGC-1-responsive promoters and nuclear receptors, GAL4-PGC-1α was functionally defective, and PGC-1β 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. Keywords: conditional knockout in mice

2007-02-08 | GSE6662 | GEO

E-GEOD-30076

Project description:Transcription profiling by array of mouse heart mutant for Ezh2

2014-07-03 | E-GEOD-30076 | ExpressionAtlas

E-GEOD-74538

Project description:Transcription profiling of midbrain samples from Ezh2 knockout mouse embryos

2016-01-08 | E-GEOD-74538 | ExpressionAtlas

E-GEOD-19517

Project description:Gene expression profiling of conditional ablation of Indian hedgehog in the mouse uterus

2015-09-08 | E-GEOD-19517 | ExpressionAtlas

E-GEOD-70681

Project description:Transcription profiling by array of Pten knockout liver cells of mouse