ELK1 ChIP-seq
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR050206.fastq.gz | Fastqsanger.gz | |||
| ERR050207.fastq.gz | Fastqsanger.gz | |||
| ERR050208.fastq.gz | Fastqsanger.gz | |||
| ERR050209.fastq.gz | Fastqsanger.gz | |||
| ERR050210.fastq.gz | Fastqsanger.gz |
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2012-08-20 | E-MTAB-830 | biostudies-arrayexpress
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.
2013-05-31 | E-MTAB-1565 | biostudies-arrayexpress
Project description:ChIP-Seq for ERK2/MAPK1 and ELK1 in human embryonic stem cells
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Project description:Estrogen Receptor alpha (ERα) is a key driver of most breast cancers, and it is the target of endocrine therapies used in the clinic to treat women with ERα positive (ER+) breast cancer. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ERα function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used to pull down the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ERα have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ERα in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.
2019-03-21 | PXD012930 | Pride
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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Project description:Cellular reprogramming using chemically defined conditions, without genetic manipulation, is a promising approach for generating clinically relevant cell types for regenerative medicine and drug discovery. However, small molecule-driven approaches for inducing lineage-specific stem cells from somatic cells across lineage boundaries have been challenging to develop. Here, we report highly efficient reprogramming of mouse fibroblasts into induced neural stem cell-like cells (ciNSLCs) using a cocktail of nine small molecules (M9). The resulting ciNSLCs closely resemble primary neural stem cells molecularly and functionally. Transcriptome analysis revealed that M9 induces a gradual and specific conversion of fibroblasts towards a neural fate. During reprogramming specific transcription factors such as Elk1 and Gli2 that are downstream of M9-induced signaling pathways bind and activate endogenous master neural genes to specify neural identity. Our study therefore provides an effective chemical approach for generating neural stem cells from mouse fibroblasts, and reveals mechanistic insights into underlying reprogramming process. Genome-wide binding of Elk1 and Gli2 was analyzed by CHIP-seq for tdMEFs from day 0 (ciNSLC), day 4 (D4), day 8 (D8) of M9-induced neural reprogramming, and ciNSLCs and pri-NPC.
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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
Project description:ELK1 ChIP-seq on human A549 For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
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