Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

FloChIP's MEF2-A data obtained with high-throughput chip

ABSTRACT: FloChIP's MEF2-A data obtained with high-throughput chip

PROVIDER: PRJEB28685 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR2804740_1.fastq.gz	Fastqsanger.gz
	ERR2804740_2.fastq.gz	Fastqsanger.gz
	ERR2804750_1.fastq.gz	Fastqsanger.gz
	ERR2804750_2.fastq.gz	Fastqsanger.gz
	ERR2804760_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 94

Similar Datasets

FloChIP's MEF2-A data obtained with high-throughput chip

Project description:By using FloChIP’s high-throughput, we ChIPed in parallel 47 chromatin cell lines with anti-mef2a antibody.

2019-11-26 | E-MTAB-7179 | biostudies-arrayexpress

FloChIP's histone mark data obtained in multiplexing mode

Project description:FloChIP's histone mark data obtained in multiplexing mode

| PRJEB35683 | ENA

FloChIP's histone mark data obtained in multiplexing mode

Project description:FloChIP's histone mark data obtained in multiplexing mode

| PRJEB28149 | ENA

FloChIP's decreasing cell number data obtained in multiplexing mode

Project description:FloChIP's decreasing cell number data obtained in multiplexing mode

| PRJEB28205 | ENA

FloChIP's sequential chip data

Project description:FloChIP's sequential chip data

| PRJEB28503 | ENA

MEF2 Activated Genes

Project description:Expression profiling in hippocampal neurons to identify genes upregulated in response to ectopic MEF2 activation by MEF2-VP16-ER Experiments were conducted to identify activity-regulated MEF2 target genes. Keywords: Gene activation time course

2009-01-12 | GSE13538 | GEO

MEF2 Regulated Genes

Project description:Expression profiling in hippocampal neurons to identify activity-regulated genes controlled by MEF2 Experiments were conducted to identify activity-regulated MEF2 target genes. Keywords: Gene knockdown and depolarization time course

2009-01-12 | GSE13537 | GEO

Novel targets for the transcription factors MEF2 in MA-10 Leydig cells

Project description:Testosterone production by Leydig cells is a tightly regulated process requiring synchronized expression of several steroidogenic genes by numerous transcription factors. Myocyte enhancer factor 2 (MEF2) is a transcription factor recently identified in somatic cells of the male gonad. In other tissues, MEF2 is an essential regulator of organogenesis and cell differentiation. So far in the testis, MEF2 was found to regulate Leydig cell steroidogenesis by controlling Nr4a1 and Star gene expression. To expand our understanding of the role of MEF2 in Leydig cells, we performed microarray analyses of MA-10 Leydig cells depleted in MEF2 and results were analyzed using the Partek and IPA softwares. Several genes were differentially expressed in MEF2-depleted Leydig cells and 15 were validated by qPCR. A large number of these genes are known to be involved in fertility, gonad morphology and steroidogenesis and include Pde8a, Por, Ahr, Bmal1, Cyp1a1, Cyp1b1, Map2k1, Tsc22d3, Nr0b2, Smad4, and Star, which were all downregulated in the absence of MEF2. In silico analyses revealed the presence of MEF2 binding sites within the first 2 kb upstream the transcription start site of the Por, Bmal1, and Nr0b2 promoters, which suggests a direct regulation by MEF2. Using transient transfections in MA-10 Leydig cells, siRNA knockdown, and a MEF2-Engrailed dominant negative, we found that MEF2 activates the Por, Bmal1 and Nr0b2 promoters and that this requires an intact MEF2 element. Our results identify novel target genes for MEF2 and define MEF2 as an important regulator of Leydig cell function and male reproduction.

2015-04-12 | GSE64128 | GEO

Cocaine Regulates MEF2 to Control Synaptic and Behavioral Plasticity

Project description:Repeated exposure to cocaine causes sensitized behavioral responses and increased dendritic spines on medium spiny neurons of the nucleus accumbens (NAc). We find that cocaine regulates myocyte enhancer factor 2 (MEF2) transcription factors to control these two processes in vivo. Cocaine suppresses striatal MEF2 activity in part through a novel mechanism involving cAMP, the regulator of calmodulin signaling (RCS), and calcineurin. We show that reducing MEF2 activity in the NAc in vivo is required for the cocaine-induced increases in dendritic spine density. Surprisingly, we find that increasing MEF2 activity in the NAc, which blocks the cocaine-induced increase in dendritic spine density, enhances sensitized behavioral responses to cocaine. Together, our findings implicate MEF2 as a key regulator of structural synapse plasticity and sensitized responses to cocaine, and suggest that reducing MEF2 activity (and increasing spine density) in NAc may be a compensatory mechanism to limit long-lasting maladaptive behavioral responses to cocaine.

2008-08-24 | GSE11939 | GEO

MRF4 negatively regulates adult skeletal muscle growth by repressing MEF2 activity

Project description:The myogenic regulatory factor MRF4 is expressed at high levels in myofibers of adult skeletal muscle, but its function is unknown. Here we show that knockdown of MRF4 in adult muscle causes hypertrophy and prevents denervation-induced atrophy. This effect is accompanied by increased protein synthesis and the widespread activation of genes involved in muscle contraction, excitation-contraction coupling and energy metabolism, many of which are known targets of MEF2 transcription factors. Genes regulated by MEF2 represent the top-ranking gene set enriched after Mrf4 RNAi, and a MEF2 reporter is inhibited by co-transfected MRF4 and activated by Mrf4 RNAi. The role of MEF2 in mediating the effect of MRF4 knockdown is supported by the finding that Mrf4 RNAi-dependent increase in fiber size is prevented by dominant negative MEF2, while constitutively active MEF2 is able to induce myofiber hypertrophy. The nuclear localization of the MEF2 co-repressor HDAC4 is impaired by Mrf4 knockdown, suggesting that MRF4 acts by stabilizing a repressor complex that controls MEF2 activity. The demonstration that fiber size in adult skeletal muscle is controlled by the MRF4-MEF2 axis opens new perspectives in the search for therapeutic targets to prevent muscle wasting, in particular sarcopenia and cachexia.

2016-07-15 | GSE67069 | GEO

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