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Myc is an important oncogene. It is considered as a transcription factor, but the function of Myc in normal or cancer cells have not been fully understood. In addition, Myc plays a role in cell proliferation and differentiation. It is also important for cell identity and stay on chromatin throughout the cell cycle. However, the inheritance of Myc is still a mystery. Here we study the function and inheritance of Myc in D. melanogaster by mapping the binding sites of Myc during interphase and mitosis using ChIP-seq. DNA sample of ChIP for Myc are collected from Kc cells in interphase or mitosis. Input sequences from previous study in the same cell type (GSM762848, GSM762849) are used as control.
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Accession Number: GSE36374 Platform: GPL9061: Illumina Genome Analyzer II (Drosophila melanogaster) GPL15334: Illumina HiSeq 1000 (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2012-03-29 Summary: ChIP-seq was performed using Drosophila Kc167 cells using antibodies against H3K4me3 to identify active promoters and H3K4me1 to identify active enhancers. H3K27ac ChIPseq was performed to identify active promoters and enhancers. Once enhancers and promoters were identified, JIL-1 and histone phosphorylation, H3K9acS10ph and H3K27acS28ph, ChIP-seq was performed to look at binding trends. JIL-1 and phosphoacetlation is found at low levels at inactive enhancers and shows increase at active enhancers and promoters. Overall Design: Here we examine histone phosphorylation by JIL-1 and acetylation of H3K27ac by CBP at transcriptionally active vs. inactive promoters and enhancers. ChIP-seq is performed in Kc167 Drosophila cells using antibodies against JIL-1, H3K27acS28ph, H3K9acS10ph, H3K4me3, H3K4me1, and H3K27ac. Contact: Name: Wendy A Kellner Organization: Emory University Laboratory: Victor Corces Deparment: Biology Address: 1510 Clifton Road Atlanta GA 30322 USA Email: wkellne@emory.edu Phone: 404-727-4250 Organization: GEO Address: USA
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Accession Number: GSE84595 Platform: GPL14601: AB SOLiD 4 System (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2016-11-22 Summary: ChIP-seq Y14 Overall Design: Y14 ChIP-seq in S2 cells Contact: Name: Saverio Brogna Organization: University Birmingham Address: Edgbaston Birmingham United Kingdom Email: s.brogna@bham.ac.uk Organization: GEO Address: USA
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Accession Number: GSE89459 Platform: GPL11203: Illumina Genome Analyzer IIx (Drosophila melanogaster) GPL13304: Illumina HiSeq 2000 (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2017-08-25 Summary: trr ChIP-seq, trr RNA-seq, G9a RNA-seq Overall Design: trr ChIP-seq profiles on 0-5 day old fly heads in two replicates and mRNA profiles of trr- and G9a mutant 0-5 days old fly heads in two and three replicates respectively. Contact: Name: Tom Koemans Organization: Radboudumc Laboratory: van Bokhoven/ Schenck Deparment: Human genetics Address: Geert Grooteplein 10 Nijmegen Netherlands Email: tom.koemans@radboudumc.nl Organization: GEO Address: USA
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Accession Number: GSE96959 Platform: GPL11203: Illumina Genome Analyzer IIx (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2017-12-13 Summary: This analysis largely reflected the genomic distribution of dBigH1 in spermatocytes since the vast majority of dBigH1-expressing cells in testes correspond to spermatocytes. In these studies, we observed that dBigH1 was not uniformely distributed across the genome. Overall Design: ChIP-Seq peak calling of dBigH1 against input sample in whole testes Contact: Name: Oscar Reina Garcia Organization: IRB Barcelona Deparment: Biostatistics and Bioinformatics Address: C/Baldiri Reixac 10 Barcelona Barcelona 08028 Spain Email: oscar.reina@irbbarcelona.org Organization: GEO Address: USA
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Accession Number: GSE39271 Platform: GPL13304: Illumina HiSeq 2000 (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2013-07-15 Summary: ChIP-seq and mRNA-seq experiments were performed to understand the role of the CLAMP protein in dosage compensation Overall Design: ChIP-seq experiments compared the binding profiles of CLAMP in male and female cells and mRNA-seq data to define the role of CLAMP in regulating genes on the X-chromosome Contact: Name: Erica Larschan Organization: Brown University Address: 185 Meeting St. Providence 02912 USA Email: Erica_Larschan@brown.edu Organization: GEO Address: USA
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ChIP-seq was performed to compare binding the genome-wide binding profile of the CLAMP transcription factor in two different Drosophila species. ChIP seq experiments compare the binding profile of CLAMP in female larvae to identify conservation of its binding sequence.
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This SuperSeries is composed of the following subset Series: GSE37027: Cell type-specific gene expression profiling of Drosophila neurons [RNA-Seq] GSE37032: Cell type-specific chromatin profiling of Drosophila neurons [ChIP-Seq] Refer to individual Series
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Accession Number: GSE27078 Platform: GPL9061: Illumina Genome Analyzer II (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2012-08-30 Summary: LID is a histone demethylase acting on H3K4me3, a mark related to transcription and found near the transcription start sites (TSS) of the genes. We analyzed where LID is localized and the effects of LID downregulation in the distribution of H3K4me3. Overall Design: Analysis of LID-binding sites in wild type, and of H3K4me3-binding sites in wild type and LID RNAi wing imaginal discs. Contact: Name: David Rossell Organization: IRB Barcelona Address: Baldiri Reixac 10 Barcelona 08028 Spain Email: david.rossell@irbbarcelona.org Organization: GEO Address: USA
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Accession Number: GSE19325 Platform: GPL9061: Illumina Genome Analyzer II (Drosophila melanogaster) Organism: Drosophila melanogaster Published on 2010-04-16 Summary: We use male gonads isolated from a Drosophila strain that allows us to obtain enough cells at their primitive status as the starting material to study the endogenous chromatin structure of undifferentiated cells using ChIP-seq. We integrate the ChIP-seq data with RNA-seq data that measures the transcriptome in a digital manner. Our genome-wide analyses indicate that the majority of differentiation genes in undifferentiated cells lack an active chromatin mark and paused Pol II; instead, they are associated with either the repressive H3K27me3 mark or no detectable mark. In order to address the possibility that distinct techniques are responsible for such a difference, we also use the Drosophila S2 cells to perform ChIP-seq and RNA-seq and compare the results directly with published work using ChIP-chip and microarray on S2 cells. For the S2 cell ChIP-chip data, we used data from the following paper: Muse GW, Gilchrist DA, Nechaev S, Shah R, Parker JS, Grissom SF, Zeitlinger J, Adelman K: RNA polymerase is poised for activation across the genome. /Nat Genet /2007, 39(12):1507-1511. The accession number for this data is: GSE6714. Overall Design: ChIP-seq: Profiling chromatin modifications using antibodies against 3 histone modifications and RNA Pol II in S2 cells Profiling chromatin structure in bam testis using antibodies against 3 histone modifications and RNA Pol II RNA-seq: Profiling transcriptome of S2 cells using RNA-seq Contact: Name: Dustin E Schones Organization: City of Hope Deparment: Cancer Biology Address: 1500 E Duarte Rd. Duarte CA 91010 USA Email: dschones@coh.org Organization: GEO Address: USA
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