5 results for chip-seq drosophila
Drosophila dKDM5/LID regulates H3K4me3 dynamics at the transcription start site of actively transcribed developmental genes
Contributors: Lloret-Llinares M, Pï¿½rez-Lluch S, Rossell D, Morï¿½n T, Ponsa-Cobas J, Auer H, Corominas M, Azorï¿½n F
ChIP-Seq in wild type and lid RNAi Drosophila melanogaster GSE40599: POLIISER5...Drosophila Melanogaster Refer to individual Series...Drosophila melanogaster GSE40599: POLIISER5 and POLIISER2 ChIP-Seq in ...Drosophila LID RNAi gene expression profiling GSE27078: LID ChIP-Seq in...ChIP-Seq in mutant RNAi LID Drosophila Melanogaster Refer to individual...Drosophila dKDM5/LID regulates H3K4me3 dynamics at the transcription start...Drosophila LID RNAi gene expression profiling GSE27078: LID ChIP-Seq in ... This SuperSeries is composed of the following subset Series: GSE26895: Drosophila LID RNAi gene expression profiling GSE27078: LID ChIP-Seq in wild type, and H3K4me3 ChIP-Seq in wild type and lid RNAi Drosophila melanogaster GSE40599: POLIISER5 and POLIISER2 ChIP-Seq in mutant RNAi LID Drosophila Melanogaster Refer to individual Series
Contributors: Duffy, David J., Krstic, Aleksandar, Halasz, Melinda, Schwarzl, Thomas, Konietzny, Anja, Iljin, Kristiina, Higgins, Desmond G., Kolch, Walter
ChIP-seq) ... Background: Retinoid therapy is widely employed in clinical oncology to differentiate malignant cells into their more benign counterparts. However, certain high-risk cohorts, such as patients with MYCN-amplified neuroblastoma, are innately resistant to retinoid therapy. Therefore, we employed a precision medicine approach to globally profile the retinoid signalling response and to determine how an excess of cellular MYCN antagonises these signalling events to prevent differentiation and confer resistance. Methods: We applied RNA sequencing (RNA-seq) and interaction proteomics coupled with network-based systems level analysis to identify targetable vulnerabilities of MYCN-mediated retinoid resistance. We altered MYCN expression levels in a MYCN-inducible neuroblastoma cell line to facilitate or block retinoic acid (RA)-mediated neuronal differentiation. The relevance of differentially expressed genes and transcriptional regulators for neuroblastoma outcome were then confirmed using existing patient microarray datasets. Results: We determined the signalling networks through which RA mediates neuroblastoma differentiation and the inhibitory perturbations to these networks upon MYCN overexpression. We revealed opposing regulation of RA and MYCN on a number of differentiation-relevant genes, including LMO4, CYP26A1, ASCL1, RET, FZD7 and DKK1. Furthermore, we revealed a broad network of transcriptional regulators involved in regulating retinoid responsiveness, such as Neurotrophin, PI3K, Wnt and MAPK, and epigenetic signalling. Of these regulators, we functionally confirmed that MYCN-driven inhibition of transforming growth factor beta (TGF-β) signalling is a vulnerable node of the MYCN network and that multiple levels of cross-talk exist between MYCN and TGF-β. Co-targeting of the retinoic acid and TGF-β pathways, through RA and kartogenin (KGN; a TGF-β signalling activating small molecule) combination treatment, induced the loss of viability of MYCN-amplified retinoid-resistant neuroblastoma cells. Conclusions: Our approach provides a powerful precision oncology tool for identifying the driving signalling networks for malignancies not primarily driven by somatic mutations, such as paediatric cancers. By applying global omics approaches to the signalling networks regulating neuroblastoma differentiation and stemness, we have determined the pathways involved in the MYCN-mediated retinoid resistance, with TGF-β signalling being a key regulator. These findings revealed a number of combination treatments likely to improve clinical response to retinoid therapy, including co-treatment with retinoids and KGN, which may prove valuable in the treatment of high-risk MYCN-amplified neuroblastoma.
Genome-wide Binding Site Analysis of FAR-RED ELONGATED HYPOCOTYL 3 Reveals Its Novel Function in Arabidopsis Development
Contributors: Ouyang X, Li J, Li G, Li B, Chen B, Shen H, Huang X, Mo X, Wan X, Lin R
ChIP-Seq data from Arabidopsis thaliana under dark and far-red light GSE30712 ... This SuperSeries is composed of the following subset Series: GSE30711: ChIP-Seq data from Arabidopsis thaliana under dark and far-red light GSE30712: Expression data from Arabidopsis thaliana under dark and far-red light Refer to individual Series
ChIP-Seq) and mRNA transcriptional profiling, we show that direct ERE ... The nuclear receptor, estrogen receptor alpha (ERα), controls the expression of hundreds of genes responsible for target cell phenotypic properties, but the relative importance of direct vs. tethering mechanisms of DNA binding has not been established. In this first report, we examine the genome-wide chromatin localization of an altered-specificity mutant ER with a DNA-binding domain deficient in binding to estrogen response element (ERE)-containing DNA (DBDmut ER) vs. wild type ERα. Using high-throughput sequencing of ER chromatin immunoprecipitations (ChIP-Seq) and mRNA transcriptional profiling, we show that direct ERE binding is required for most (75%) estrogen-dependent gene regulation and 90% of hormone-dependent recruitment of ER to genomic binding sites. De novo motif analysis of the chromatin binding regions in MDA-MB-231 human breast cancer cells defined unique transcription factor profiles responsible for genes regulated through tethering vs. direct DNA (ERE) binding, with Runx motifs enriched in ER-tethered sites. We confirmed a role for Runx1 in mediating ERa genomic recruitment and regulation of tethering genes. Our findings delineate the contributions of ERE binding vs. binding through response elements for other transcription factors in chromatin localization and ER-dependent gene regulation, paradigms likely to underlie the gene regulatory actions of other nuclear receptors as well. This SuperSeries is composed of the following subset Series: GSE22593: WT and DBDmut Breast Cancer Cells GSE22609: Genome-Wide Maps of WT and DBDmut Estrogen Receptor in Human Breast Cancer Cells Refer to individual Series
Contributors: Jessica Cox, Corey Harper
... This dataset contains 4 files: 1. A .csv containing 29,105 sentences from CC-BY papers that contain citations ("pygothamCleanDataset.csv"). 2. A community edition databricks notebook to process and explore the data as .dbc 3. A community edition databricks notebook to view in HTML. 3. Pygotham slides in PDF format.