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DNA microarrays (time course) of MEFs transduced with SKO plus HDAC7 or MEF2C

ABSTRACT: Overexpression HDAC7 can enhance iPS efficiency in SKO by supressing MEF2 factors We used microarrays to identify changes induced by overexpression of HDAC7 or MEF2C. MEFs were transduced with SKO plus HDAC7 or MEF2C compared to SKO plus empty vector(Flag), GFP as controls. TRIZOL cell lysates were prepared from D6 and D10.

ORGANISM(S): Mus musculus

SUBMITTER: Duanqing Pei

PROVIDER: E-GEOD-23692 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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DNA microarrays (time course) of MEFs transduced with SKO plus HDAC7 or MEF2C

Project description:Overexpression HDAC7 can enhance iPS efficiency in SKO by supressing MEF2 factors We used microarrays to identify changes induced by overexpression of HDAC7 or MEF2C.

2011-08-18 | GSE23692 | GEO

MEF2A, MEF2C, and MEF2D Interactomes in Mouse MA-10 Leydig Cells

Project description:In steroidogenic Leydig cells, MEF2A, MEF2C, and MEF2D are key regulators of genes involved in steroid hormone synthesis, reproductive function, and oxidative stress defense. Here we used TurboID proximity-mediated biotinylation to map the protein-protein interaction networks of MEF2A, MEF2C, and MEF2D in mouse MA-10 Leydig cells. Interactions were captured under both basal (unstimulated) and forskolin-stimulated conditions to examine differences in the MEF2 interactomes in relation to steroidogenesis. This dataset provides insights into MEF2-related signalling pathways and the functional landscape of MEF2 transcription factors in Leydig cells.

2024-11-15 | MSV000096432 | MassIVE

Mus musculus

Project description:DNA microarrays (time course) of MEFs transduced with SKO plus HDAC7 or MEF2C

| PRJNA130863 | ENA

Transcriptome profiling of murine aortic endothelium deleted for the transcription factor Mef2c

Project description:Laminar flow on endothelial cells in vitro activates MEF2 transcription factors to induce expression of atheroprotective genes. Here we sought to establish in vivo MEF2 functions in the endothelium through endothelial-specific deletion of Mef2c. Our results show that endothelial Mef2c regulates migration of vascular smooth muscle from the tunica media into the intima through fenestrations in the internal elastic lamina. Moreover, Mef2c regulates actin stress fiber formation in the endothelium. To investigate Mef2c-dependent targets in the endothelium, we perform transcriptome profiling on RNA isolated from the aortic endothelium with or without Mef2c deletion.

2017-05-31 | GSE97089 | GEO

Expression data from HUVEC adenovirally overexpressing MEF2C

Project description:The transcription factor MEF2C is specifically induced by VEGF in endothelial cells. To delineate target genes of MEF2C in endothelial cells, which might be important during angiogenesis also, MEF2C was overexpressed adenovirally in human umbilical vein endothelial cells (HUVECs) over a period of 8 to 32 hours. Expression data should be compared to control infected cells, to discriminate against virally induced genes, and should be further compared to HUVECs infected with an adenovirus encoding for a dominant-negative form of MEF2. HUVECs of the same batch, passage 3 were infected with Ad.con, Ad.MEF2C or Ad.DNMEF2 for 8, 16 or 32 hours for RNA extraction and hybridization on Affymetrix microarrays.

2013-06-01 | E-GEOD-46279 | biostudies-arrayexpress

Expression data from HUVEC adenovirally overexpressing MEF2C

2013-06-01 | GSE46279 | GEO

Gene expression analysis to identify Mef2c/d target genes in B-cell progenitors

Project description:The sequential activation of distinct developmental gene networks governs the ultimate identity of a cell, but the mechanisms by which downstream programs are activated are incompletely understood. The preB-cell receptor (preBCR) is an important checkpoint of B-cell development and essential for a preB-cell to traverse into an immature B-cell. Here, we show that activation of Mef2 transcription factors by preBCR is necessary for initiating the subsequent genetic network. We demonstrate that B-cell development is blocked at the preB-cell stage in mice deficient for Mef2c and Mef2d transcription factors and that preBCR signaling enhances the transcriptional activity of Mef2c/d through phosphorylation by the ERK5 mitogen activating kinase. This activation is instrumental in inducing KrÃ¼ppel-like factor 2 and several immediate early genes of the AP1 and Egr family. Finally, we show that Mef2 proteins cooperate with the products of their target genes (Irf4 and Egr2) to induce secondary waves of transcriptional regulation. Our findings uncover a novel role for Mef2c/d in coordinating the transcriptional network that promotes early B-cell development. RNA-seq experiments were performed from Mef2c/d knockout proB-cells versus control cells to identify genes regulated by Klf2

2015-12-14 | E-GEOD-73561 | biostudies-arrayexpress

Genome-wide mapping of Mef2c-bound sites in early B-cell progenitors

Project description:The sequential activation of distinct developmental gene networks governs the ultimate identity of a cell, but the mechanisms by which downstream programs are activated are incompletely understood. The preB-cell receptor (preBCR) is an important checkpoint of B-cell development and essential for a preB-cell to traverse into an immature B-cell. Here, we show that activation of Mef2 transcription factors by preBCR is necessary for initiating the subsequent genetic network. We demonstrate that B-cell development is blocked at the preB-cell stage in mice deficient for Mef2c and Mef2d transcription factors and that preBCR signaling enhances the transcriptional activity of Mef2c/d through phosphorylation by the ERK5 mitogen activating kinase. This activation is instrumental in inducing KrÃ¼ppel-like factor 2 and several immediate early genes of the AP1 and Egr family. Finally, we show that Mef2 proteins cooperate with the products of their target genes (Irf4 and Egr2) to induce secondary waves of transcriptional regulation. Our findings uncover a novel role for Mef2c/d in coordinating the transcriptional network that promotes early B-cell development. ChIP-seq experiments were performed in the proB-cell line BMiFLT3(15-3) to identify Mef2c-bound sites in early B-cell progenitors.

2015-12-14 | E-GEOD-73453 | biostudies-arrayexpress

MEF2C Protein Isoform Transition to a Repressor Variant is Linked to Development of Heart Failure

Project description:The transcription factor MEF2C has been implicated in the pathogenesis of cardiac remodeling and heart failure. The underlying mechanisms of the MEF2C detrimental effects still remain elusive. MEF2C is unique among the MEF2 family in that alternative splice acceptors in the last exon give forms that include or exclude a short domain, which has an inhibitory effect on the MEF2C activity. Objective: To identify if MEF2Cγ+ repressor variant has a role in the cardiac detrimental effects of MEF2C. Conclusions: We conclude that upregulation of MEF2Cγ+ in adult hearts causes cardiac pathogenic features through dysregulation of cell cycle and dedifferentiation of cardiomyocytes.

2020-01-22 | GSE99748 | GEO

Genome-wide mapping of Mef2c-bound sites in early B-cell progenitors

Project description:The sequential activation of distinct developmental gene networks governs the ultimate identity of a cell, but the mechanisms by which downstream programs are activated are incompletely understood. The preB-cell receptor (preBCR) is an important checkpoint of B-cell development and essential for a preB-cell to traverse into an immature B-cell. Here, we show that activation of Mef2 transcription factors by preBCR is necessary for initiating the subsequent genetic network. We demonstrate that B-cell development is blocked at the preB-cell stage in mice deficient for Mef2c and Mef2d transcription factors and that preBCR signaling enhances the transcriptional activity of Mef2c/d through phosphorylation by the ERK5 mitogen activating kinase. This activation is instrumental in inducing Krüppel-like factor 2 and several immediate early genes of the AP1 and Egr family. Finally, we show that Mef2 proteins cooperate with the products of their target genes (Irf4 and Egr2) to induce secondary waves of transcriptional regulation. Our findings uncover a novel role for Mef2c/d in coordinating the transcriptional network that promotes early B-cell development.

2015-12-14 | GSE73453 | GEO

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