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Cardiac over-expression of Med13

ABSTRACT: Med13 cardiac over-expression regulates cardiac gene expression and metabolism

ORGANISM(S): Mus musculus

PROVIDER: GSE35902 | GEO | 2012/02/18

SECONDARY ACCESSION(S): PRJNA155687

REPOSITORIES: GEO

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Cardiac over-expression of Med13

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Cardiac over-expression of Med13, non-cardiac tissue analysis

Project description:Med13 cardiac over-expression regulates obesity. Liver, WAT and BAT from alphaMHC-Med13 TG mice was analyzed

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Cardiac over-expression of Med13, non-cardiac tissue analysis

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Med13 overexpression

Project description:This SuperSeries is composed of the following subset Series: GSE35902: Cardiac over-expression of Med13 GSE35903: Cardiac over-expression of Med13, non-cardiac tissue analysis Med13 cardiac transgenic mice were back-crossed 4 or more generations to C57Bl6 mice. Refer to individual Series

2012-02-18 | E-GEOD-35904 | biostudies-arrayexpress

Regulation of cardiac transcription by thyroid hormone and Med13

Project description:Purpose: The objective of this study was to determine cardiac transcriptional pathways regulated in response to 1.) hypothyroidism and re-establishment of a euthyroid state and 2.) Med13-dependent cardiac transcriptional pathways regulated in response to hypothyroidism and re-establishment of a euthyroid state

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Cardiomyocyte-specific Deletion of Med13 and Med13L Results in Dysregulated Gene Expression and Lethal Heart Failure

Project description:Background: Previous studies have linked mutations in the Mediator complex, specifically Mediator 13 (Med13) and Mediator 13-like (Med13L), with both congenital heart defects and cardiovascular diseases. Med13 and Med13L are mutually exclusive paralogs within the kinase submodule of the Mediator complex that have been shown to have partially redundant functions in embryonic development and transcription, but their combined roles have not been investigated in the adult heart. We investigated the critical yet redundant roles of Med13 and Med13L in adult murine cardiomyocytes for basal cardiac function. Methods: We generated an inducible Med13 and Med13L cardiomyocyte-specific knockout mouse model to investigate Med13 and Med13L regulation of cardiac function and transcription. We performed RNAseq on mice four weeks after the start of tamoxifen to identify changes in gene expression. Differentially expressed genes were compared across cardiac knockouts of Med13/13L, Med13, Med12, Med1, and Med30 elucidating similar mechanisms of cardiac dysfunction. Results: Med13/13L knockout resulted in decreased cardiac function leading to lethal heart failure in a median timeframe of 6 weeks from the start of tamoxifen. There is significant gene dysregulation after Med13/13L knockout with similar gene dysregulation of fibrotic pathways and calcium handling across Mediator cardiac knockouts. Conclusions: Med13 and Med13L function partially redundantly within the heart to maintain basal cardiac function and transcription, as well as redundancies within cardiac phenotypes related to mediator complex disruptions.

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Effect of over expression of MED13 IDR in human osteosarcoma U2OS cell line

Project description:Effect of over expression of MED13 IDR in human osteosarcoma U2OS cell line

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Regulation of cardiac transcription by thyroid hormone and Med13

Project description:Regulation of cardiac transcription by thyroid hormone and Med13

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Mus musculus

Project description:Cardiac over-expression of Med13

| PRJNA155687 | ENA

Effect of over expression of MED13 IDR in human osteosarcoma U2OS cell line

Project description:The eukaryotic transcriptional Mediator comprises a large Core (cMED) and a dissociable CDK8 kinase module (CKM). cMED recruits RNA polymerase II (Pol II) and promotes pre-initiation complex formation in a manner repressed by the CKM through mechanisms presently unknown. Herein we report cryo-electron microscopy structures of the complete human Mediator and its CKM. Combined with biochemical and functional analyses, these structures provide a mechanistic framework to explain the basis for CKM-mediated repression of cMED function. The CKM binds to cMED at multiple sites through both MED12 and a large intrinsically disordered region (IDR) in MED13. The MED13 IDR blocks Pol II/MED26 recruitment onto cMED by direct occlusion of their corresponding binding sites, leading to functional repression of cMED-dependent transcription. Notably, the CKM is anchored to the cMED Hook, positioning CDK8 downstream and proximal to the transcription start site, which sheds new light on its stimulatory function in post-initiation events.

2024-12-01 | GSE250492 | GEO

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