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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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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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.
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Project description:Arabidopsis thaliana CHIP, CHIP [Source:UniProtKB/TrEMBL;Acc:A0A178VGJ7], is differentially expressed in 100 experiment(s);
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Project description:Arabidopsis thaliana CHIP, CHIP [Source:UniProtKB/TrEMBL;Acc:A0A178VGJ7], is expressed in 13 baseline experiment(s);
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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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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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