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Genome wide maps of ELK1 bingding sites in HDFs control and mechanic loading groups.

ABSTRACT: Genome wide maps of ELK1 bingding sites in HDFs control and mechanic loading groups.

PROVIDER: PRJNA489249 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7782792_1.fastq.gz	Fastqsanger.gz
	SRR7782792_2.fastq.gz	Fastqsanger.gz
	SRR7782793_1.fastq.gz	Fastqsanger.gz
	SRR7782793_2.fastq.gz	Fastqsanger.gz
	SRR7782794_1.fastq.gz	Fastqsanger.gz

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Genome wide maps of ELK1 bingding sites in HDFs control and mechanic loading groups.

Project description:HDFs were cultured for 24 hrs for adhesion and to reach 50-70% confluence before mechanical tension was applied. Cyclic mechanical stretch (CMS) with a 0.5-Hz sinusoidal curve at 10-20% elongation was applied using a Flexcell○RFX-5000TM Tension System during the stretching. Cells were harvested immediately after the application of CMS stimulation was completed. Control cells were cultured on the same plates in the same incubator with no stretching.

2019-08-27 | GSE119433 | GEO

ELK1 ChIP-seq

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Small molecular ALA targets ELK1 to balance human neutrophil and erythroid differentiation

Project description:Alpha lipoic acid is reported to inhibit neutrophil lineage determination by targeting transcription factor ELK1 in granulocyte-monocyte progenitors. Here, we provide new evidence of alpha lipoic acid in promoting erythroid differentiation by targeting transcription factor ELK1 in CD34+CD371– hematopoietic stem progenitor cells. Over expression of both L-ELK1 and S-ELK1 greatly inhibit erythroid cell differentiation, but not knocking down of ELK1. Thus, RNAseq of CD34+CD123+CD38+CD371– HSPCs is performed to dissect the molecular mechanism of ELK1 in blocking erythrocyte differentiation.

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ELK1 ChIP-seq

Project description:Chromatin immunoprecipitation of ELK1 in MCF10A cells detected by SOLiD sequencing

2012-08-20 | E-MTAB-830 | biostudies-arrayexpress

siRNA ELK1 depletion and EGF stimulation

Project description:ELK1 is a well-known target of the ERK branch (EGF-responsive) of the MAP kinase pathway. This transcription profiling experiment studied the effects of ELK1 depletion by siRNA and subsequent EGF stimulation.

2012-07-20 | E-MEXP-3407 | biostudies-arrayexpress

CHD8 and ELK1 cooperativity regulate cellular sensitivity to MAPK/ERK pathway

Project description:The chromodomain helicase DNA binding protein CHD8 is among the most frequently found de-novo mutations in autism. Unlike other autism-risk genes, CHD8 mutations appear to be fully penetrant. Despite this prominent disease involvement, relatively little is known about its molecular function. Based on sequence homology, CHD8 is believed to be a chromatin regulator but mechanisms for its genomic targeting and its function on chromatin are unclear. Here, we developed a human cell model carrying conditional CHD8 loss-of-function alleles. Remarkably, while undifferentiated human embryonic stem (ES) cells required CHD8 for survival, postmitotic neurons survived following CHD8 depletion. Chromatin accessibility revealed that CHD8 is a highly potent and general chromatin activator, enhancing transcription of its direct target genes. We also found that CHD8 genomic binding in human neurons was significantly enriched at ELK1 DNA binding motifs as previously found in other cell types. Given its prominent role as effector molecule of the MAPK/ERK pathway, we decided to further explore its relationship with CHD8. ELK1 motif-containing CHD8 binding sites showed a higher degree of chromatin opening function of CHD8 than other CHD8 binding sites. Moreover, ELK1 was required for CHD8 binding to Elk1-containing sites, but not other sites. Finally, the anti-apoptotic function of CHD8 in human ES cells could be rescued by depletion of ELK1 and the enhancement of neurogenesis by ELK1 was dependent on presence of CHD8. In summary, our results establish a clear role of CHD8 for chromatin opening and transcriptional activation and a molecular and functional interdependence of CHD8 and ELK1. These data imply the involvement of the MAPK/ERK pathway effector ELK1 in the pathogenesis of autism caused by CHD8 mutations.

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ELK1 and NFYA knockdown in MBA-MD-231 cell line

Project description:Dual-color transcriptional profiling of siRNA-transfected cells, targeting ELK1 and NFYA, versus mock-transfected cells.

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Project description:The purpose of this protocol is to develop a detailed MRI technique and haemodynamic maps enabling early detection of colorectal metastases in the liver.

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Elk1 Directs a Critical Component of Growth Signaling by the Androgen Receptor in Prostate Cancer

Project description:Elk1 directs selective gene induction that is a substantial and critical component of growth signaling by AR in PC cells.

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Project description:The ERK/MAPK signal transduction cascade is one of the key pathways regulating proliferation and differentiation in development and disease. In human embryonic stem cells (hESCs), ERK signaling is required for their self-renewing property. Here we studied the convergence of the ERK signaling cascade at the DNA by mapping genome-wide kinase-chromatin interactions for ERK2 in hESCs. We observe that ERK2 targets genes coding for small RNAs, histones, and genes involved in cellular metabolism and cell cycle. We find that the transcription factor ELK1 is essential in hESCs and that ERK2 co-occupies promoters bound by ELK1. Strikingly, promoters bound by ELK1 without ERK2 are occupied by Polycomb group proteins that repress genes involved in lineage commitment. In summary, we propose a model where extracellular signaling-stimulated proliferation and intrinsic repression of differentiation is integrated to maintain the identity of hESCs.

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