Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MEF2C interaction profiles (4C-seq) in SH-SY5Y and HEK cell lines

ABSTRACT: To characterize enhancer elements regulating the MEF2C gene during neurodevelopment, we performed among others Circularized Chromosome Conformation Capture (4C) sequencing in a neuronal cell line, SH-SY5Y, and a non-neuronal control, HEK. We found that, in a neuronal cell line, the MEF2C promoter interacts with several putative enhancer elements in its upstream region, forming a complex interaction network. Moreover, these interactions are completely absent in HEK cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE121549 | GEO | 2018/10/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

MEF2C interaction profiles (4C-seq) in SH-SY5Y and HEK cell lines

Project description:MEF2C interaction profiles (4C-seq) in SH-SY5Y and HEK cell lines

| PRJNA497741 | ENA

MEF2C hypofunction in neuronal and neuroimmune populations produces MEF2C haploinsufficiency syndrome behaviors in mice

Project description:Microdeletions of the MEF2C gene are linked to a syndromic form of autism termed MEF2C haploinsufficiency syndrome (MCHS). Here, we show that MCHS-associated missense mutations cluster in the conserved DNA binding domain and disrupt MEF2C DNA binding. DNA binding-deficient global Mef2c heterozygous mice (Mef2c-Het) display numerous MCHS-like behaviors, including autism-related behaviors, as well as deficits in cortical excitatory synaptic transmission. We find that hundreds of genes are dysregulated in Mef2c-Het cortex, including significant enrichments of autism risk and excitatory neuron genes. In addition, we observe an enrichment of upregulated microglial genes, but not due to neuroinflammation in the Mef2c-Het cortex. Importantly, conditional Mef2c heterozygosity in forebrain excitatory neurons reproduces a subset of the Mef2c-Het phenotypes, while conditional Mef2c heterozygosity in microglia reproduces social deficits and repetitive behavior. Together our findings suggest that MEF2C regulates typical brain development and function through multiple cell types, including excitatory neuronal and neuroimmune populations.

2020-10-24 | GSE139419 | GEO

Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience II

Project description:Here we report that activation of cyclic GMP-AMP synthase (cGAS) diminishes cognitive resilience by decreasing the neuronal transcriptional network of myocyte enhancer factor 2c (MEF2C) through type I interferon (IFN-I) signaling. Pathogenic tau activates cGAS and IFN-I responses in microglia, in part mediated by cytosolic leakage of mitochondrial DNA. Genetic ablation of cGAS in tauopathy mice diminished microglial IFN-I response, preserved synapse integrity and plasticity, and protected against cognitive impairment without affecting the pathogenic tau load. cGAS ablation enhanced, while activation of IFN-I downregulated, neuronal MEF2C expression network linked with cognitive resilience in AD.

2023-04-26 | GSE226381 | GEO

CD44s transfection in HEK cells

2014-12-05 | GSE63862 | GEO

MEF2C hypofunction in neuronal and neuroimmune populations produces MEF2C haploinsufficiency syndrome behaviors in mice

Project description:MEF2C hypofunction in neuronal and neuroimmune populations produces MEF2C haploinsufficiency syndrome behaviors in mice

| PRJNA579584 | ENA

CD44s transfection in HEK cells

Project description:In order to understand the transcriptional effects of CD44s expression in a cell line that does not express CD44 in its native form we transfected CD44s into HEK cells and measured the transcriptional chances compared to native HEK cells Three biological replicates from each condition (native HEK cells and CD44s transfected cells) were measured using Affymetrix arrays

2014-12-05 | E-GEOD-63862 | biostudies-arrayexpress

RNA-binding protein AUF1 promotes myogenesis by regulating MEF2C expression levels

Project description:The mammalian RNA-binding protein AUF1 (AU-binding factor 1, also known as heterogeneous nuclear ribonucleoprotein D, hnRNP D) binds to numerous mRNAs and influences their post-transcriptional fate. Given that many AUF1 target mRNAs encode muscle-specific factors, we investigated the function of AUF1 in skeletal muscle differentiation. In mouse C2C12 myocytes, where AUF1 levels rise at the onset of myogenesis and remain elevated throughout myocyte differentiation into myotubes, RIP (RNP immunoprecipitation) analysis indicated that AUF1 binds prominently to Mef2c (myocyte enhancer factor 2c) mRNA, which encodes the key myogenic transcription factor Mef2c. By performing mRNA half-life measurements and polysome distribution analysis, we found that AUF1 associated with the 3’UTR of Mef2c mRNA and promoted Mef2c translation without affecting Mef2c mRNA stability. In addition, AUF1 promoted Mef2c gene transcription via a lesser-known role of AUF1 in transcriptional regulation. Importantly, lowering AUF1 delayed myogenesis, while ectopically restoring Mef2c expression levels partially rescued the impairment of myogenesis seen after reducing AUF1 levels. We propose that Mef2c is a key effector of the myogenesis program promoted by AUF1. Keywords: ribonucleoprotein complex; post-transcriptional gene regulation; muscle cell differentiation; myocytes; mRNA translation; mRNA stability; post-transcriptional gene regulation; transcriptome

2014-12-22 | GSE58259 | GEO

Tumorigenic effects of TLX over-expression in HEK 293T cells

Project description:Transcriptomic profiling to investigate the effect of TLX overexpression with an inducible vector system in the HEK 293T cell line

2021-01-21 | GSE120893 | GEO

CRISPR modeling reveals transcriptional and functional changes associated with structural variant disruption to MEF2C and 5q14.3 topological organization in neuronal lineages

Project description:Chromosome 5q14.3 harbored an unusual but genome-wide significant excess of noncoding BCA breakpoints that did not directly disrupt MEF2C. This distribution of breakpoints in proximity but not directly disruptive to MEF2C was further supported by microdeletions in NDD cases reported in DECIPHER34. In considering the landscape of de novo SVs across the 5q14.3 locus in NDD cases, the primary unifying thread appears to be distal boundary disruption. Taken together, these data provide compelling clinical genetic and statistical genomics evidence suggesting that both direct disruption of MEF2C and alterations to this gene’s encompassing 3D regulatory architecture may result in comparable molecular mechanisms in NDD cases. Motivated by these findings, we have performed a systematic molecular dissection of the 5q14.3 locus to quantify the transcriptomic and electrophysiological effects of MEF2C LoF in human neural derivatives. Through the generation of an allelic series of CRISPR-engineered human induced pluripotent stem cell (hiPSC)-derived neural stem cells (NSCs) and glutamatergic neurons (iNs), we interrogated the impact of enhancer, TAD boundary, and loop boundary deletion on local genome organization, local expression effects on MEF2C, and global transcriptional signatures. Our analyses reveal that direct MEF2C alteration results in both transcriptional and functional changes to the synapse. Moreover, we find that disruption of the distal boundary of the MEF2C-containing loop is insufficient to produce indirect MEF2C haploinsufficiency. By contrast, disruption of the proximal boundary of the same 3D structure results in haploinsufficiency of MEF2C that is comparable to direct gene disruption. Overall, these data suggest that the effects of direct and indirect MEF2C disruption contribute to cell type-specific alterations on neuronal functions that converge on synaptic deficits in neurodevelopment.

2022-06-10 | GSE204778 | GEO

MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [mutant MEF2C]

Project description:In acute myeloid leukemia, chemotherapy resistance remains prevalent and poorly understood. Using functional proteomics of patient AML specimens, we identified MEF2C S222 phosphorylation as a specific marker of primary chemoresistance. We found that transgenic Mef2cS222A/S222A mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by MLL-AF9. MEF2C phosphorylation was required for leukemia stem cell maintenance, induced by MARK kinases in cells, and blocked by selective MARK inhibitor MRT199665, which caused apoptosis of MEF2C-activated human AML cell lines and primary patient specimens, but not those lacking MEF2C. These findings identify signaling-dependent dysregulation of transcription factor control as a determinant of therapy response in AML, with immediate potential for improved diagnosis and therapy for this disease.

2018-07-23 | GSE94453 | 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