DNA Binding Signatures of the Myocyte Enhancer Factor-2B
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA478393 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11773025.fastq.gz | Fastqsanger.gz | |||
| SRR11773026.fastq.gz | Fastqsanger.gz | |||
| SRR11773027.fastq.gz | Fastqsanger.gz | |||
| SRR11773028.fastq.gz | Fastqsanger.gz | |||
| SRR11773029.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:DNA binding function of the myocyte enhancer factor-2B (MEF2B) is achieved through its unique capability of binding to target sites with a degenerate motif, while still functioning as a gene-specific transcriptional regulator. MEF2B-DNA recognition likely involves elements beyond the sequence of letters, aspects that are crucial to understand, particularly given recent evidence suggesting MEF2B regulatory role across a number of tissues and involvement with B-cell lymphoma. By coupling structural information, SELEX-seq and computational analysis, we were able to deduce sequence and shape determinants of MEF2B target sites at a high-throughput scale in vitro, based on which modeling binding affinities further exposed sequence-dependent shape patterns. The resulting binding signature of MEF2B reveals intricacies of DNA recognition mechanisms that, different from other TFs, sets it as a unique TF that combines base readout at the edges and shape readout at the center of its degenerate core-binding site.
2020-07-21 | GSE116401 | GEO
Project description:Myocyte enhancer factor 2 contributes as a transcription factor to cardiac remodeling processes. We wanted to link and compare known myocyte enhancer factor 2 targets to overall targets. Therefore, we used a model of neonatal rat cardiomyocytes and precipitated sheared chromatin samples with 5µg of MEF2 Ab.
2017-11-21 | E-MTAB-6213 | biostudies-arrayexpress
Project description:Myocyte enhancer factor-2B (MEF2B) has the unique capability of binding to its DNA target sites with a degenerate motif, while still functioning as a gene-specific transcriptional regulator. Identifying its DNA targets is crucial given regulatory roles exerted by members of the MEF2 family and MEF2B's involvement in B-cell lymphoma. Analyzing structural data and SELEX-seq experimental results, we deduced the DNA sequence and shape determinants of MEF2B target sites on a high-throughput basis in vitro for wild-type and mutant proteins. Quantitative modeling of MEF2B binding affinities and computational simulations exposed the DNA readout mechanisms of MEF2B. The resulting binding signature of MEF2B revealed distinct intricacies of DNA recognition compared to other transcription factors. MEF2B uses base readout at its half-sites combined with shape readout at the center of its degenerate motif, where A-tract polarity dictates nuances of binding. The predominant role of shape readout at the center of the core motif, with most contacts formed in the minor groove, differs from previously observed protein-DNA readout modes. MEF2B, therefore, represents a unique protein for studies of the role of DNA shape in achieving binding specificity. MEF2B-DNA recognition mechanisms are likely representative for other members of the MEF2 family.
| S-EPMC7470950 | biostudies-literature
Project description:ChIPseq of Myocyte Enhancer Factor 2 in neonatal rat cardiomyocytes to distinguish MEF2 binding sites
| PRJEB23434 | ENA
Project description:Myocyte enhancer factor 2A (MEF2A) is a crucial transcritional activator which plays diverse roles in the control of cell growth, survival, apoptosis and inflammation etc. To expore the gene expression signature of human coronary artery endothelial cells (HCAEC) in reponse to inhibition of MEF2A， we have employed whole genome microarray expression profiling as a discovery platform to identify genes with important functional role in HCAEC. Three independent groups of HCAEC transfected with MEF2A specific siRNA were separately performed. Three MEF2A specific siRNA groups were indicated as 1527-1, 1527-2 and 1527-3, and the mixed control group was designated as NC.
2019-01-01 | GSE114114 | GEO
Project description:MEF2 (myocyte enhancer factor 2) proteins are a small family of transcription factors that play pivotal roles in striated muscle differentiation, development, and metabolism, in neuron survival and synaptic formation, and in lymphocyte selection and activation. Products of the four mammalian MEF2 genes, MEF2A, MEF2B, MEF2C, and MEF2D, are expressed with overlapping but distinct temporospatial patterns. Toward analysis of MEF2A functions and the determinants of its regulated expression, we have mapped and begun studies of the transcriptional control regions of this gene. Heterogeneous 5'-untranslated regions of MEF2A mRNAs result from use of alternative promoters and splicing patterns. The two closely approximated TATA-less promoters are approximately 65 kb upstream of the exon containing the sole initiation codon. Ribonuclease protection and primer extension assays show that each promoter is active in various adult tissues. A canonical MEF2 site overlies the major promoter 1 transcription start site. This element specifically binds MEF2 factors, including endogenous nuclear MEF2A according to chromatin immunoprecipitation studies, and is critical to MEF2A transcription in myocytes. The site exerts reciprocal control of the alternative promoters, silencing promoter 1 and activating promoter 2 under some conditions. Erk5 and p38 MAPK signaling stimulate MEF2A expression by activating both promoters from the MEF2 element. MEF2A transcription is therefore subject to positive or negative regulation by its protein products, depending on signaling activities that influence MEF2 factor trans-activity. The sole MEF2 gene of the cephalochordate amphioxus has a similar regulatory region structure, suggesting that this mode of autoregulatory control is conserved among higher metazoan MEF2 genes.
| S-EPMC2447642 | biostudies-literature
Project description:Methylomonas sp. 2B strain:2B Genome sequencing
| PRJNA1169796 | ENA
Project description:Streptococcus equinus 2B strain:2B Genome sequencing and assembly
| PRJNA223471 | ENA
Project description:Myocyte enhancer factor 2A (MEF2A) is a transcription factor that plays a critical role in cell proliferation, differentiation and apoptosis. In contrast to the wide characterization of its regulation mechanism in mammalian skeletal muscle, its role in chickens is limited. Especially, its wide target genes remain to be identified. Therefore, we utilized Cleavage Under Targets and Tagmentation (CUT&Tag) technology to reveal the genome-wide binding profile of MEF2A in chicken primary myoblasts thus gaining insights into its potential role in muscle development. Our results revealed that MEF2A binding sites were primarily distributed in intergenic and intronic regions. Within the promoter region, although only 8.87% of MEF2A binding sites were found, these binding sites were concentrated around the transcription start site (TSS). Following peak annotation, a total of 1903 genes were identified as potential targets of MEF2A. Gene Ontology (GO) enrichment analysis further revealed that MEF2A target genes may be involved in the regulation of embryonic development in multiple organ systems, including muscle development, gland development, and visual system development. Moreover, a comparison of the MEF2A target genes identified in chicken primary myoblasts with those in mouse C2C12 cells revealed 388 target genes are conserved across species, 1515 target genes are chicken specific. Among these conserved genes, ankyrin repeat and SOCS box containing 5 (ASB5), transmembrane protein 182 (TMEM182), myomesin 2 (MYOM2), leucyl and cystinyl aminopeptidase (LNPEP), actinin alpha 2 (ACTN2), sorbin and SH3 domain containing 1 (SORBS1), ankyrin 3 (ANK3), sarcoglycan delta (SGCD), and ORAI calcium release-activated calcium modulator 1 (ORAI1) exhibited consistent expression patterns with MEF2A during embryonic muscle development. Finally, TMEM182, as an important negative regulator of muscle development, has been validated to be regulated by MEF2A by dual-luciferase and quantitative real-time PCR (qPCR) assays. In summary, our study for the first time provides a wide landscape of MEF2A target genes in chicken primary myoblasts, which supports the active role of MEF2A in chicken muscle development.
| S-EPMC11345569 | biostudies-literature
Project description:Premature ventricular contractions (PVCs) are common in the general population, and frequent PVCs may result in the poor quality of life or even the damage of cardiac function. We examined the efficacy and safety of a traditional Chinese medicine Wenxin Keli for the treatment of frequent PVCs among a relatively large Chinese cohort.We performed a randomized, double-blind, placebo-controlled, parallel-group, multicenter trial. A total of 1200 eligible participants were randomly assigned in a ratio of 1:1 to receive Wenxin Keli or the placebo for 4 weeks. The primary and secondary endpoint was the change of PVC numbers and PVC-related symptoms after a 4-week treatment compared with baseline, respectively. In addition, vital signs, laboratory values, and electrocardiographic parameters were assessed in a safety analysis.At the initial evaluation, no significant differences in the baseline characteristics were observed between the Wenxin Keli group and the placebo group. A smaller number of PVCs was observed after the 4-week treatment than at baseline, in both the Wenxin Keli group (5686 ± 5940 vs. 15,138 ± 7597 beats/d, P < 0.001) and the placebo group (10,592 ± 8009 vs. 14,529 ± 5929 beats/d, P < 0.001); moreover, the Wenxin Keli group demonstrated a significantly greater reduction in the frequency of PVCs than the placebo group (P < 0.001). In a full analysis set, patients in the Wenxin Keli group exhibited significantly higher total effective responses in the reduction of PVCs compared to those in the placebo group (83.8% vs. 43.5%,P < 0.001). The per-protocol analysis yielded similar results (83.0% vs. 39.3%,P < 0.001). Treatment with Wenxin Keli also demonstrated superior performance compared to the placebo with respect to PVC-related symptoms. No severe adverse effects attributable to Wenxin Keli were reported.Wenxin Keli treatment effectively reduced the overall number of PVCs and alleviated PVC-related symptoms in patients without structural heart diseases and had no severe side effects.
| S-EPMC4736860 | biostudies-literature