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Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [ChIP-Seq]

ABSTRACT: We performed genome-wide DNaseI hypersensitive site in FLT3-ITD and WT patient samples. We report corresponding gene expression, promoter methylation patterns of differential DHSs as well as differentially occupied TF binding motifs using surrounding DNAseI cut profiles. We examined association patterns of FLT3 ITD and WT AMLs and found that FLT3-ITD signaling is associated with common gene expression and chromatin signature. Examination of Runx1 binding sites in FLT3 ITD AML.

ORGANISM(S): Homo sapiens

SUBMITTER: Pierre Cauchy

PROVIDER: E-GEOD-64862 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [DNAse-Seq]

Project description:We performed genome-wide DNaseI hypersensitive site in FLT3-ITD and WT patient samples. We report corresponding gene expression, promoter methylation patterns of differential DHSs as well as differentially occupied TF binding motifs using surrounding DNAseI cut profiles. We examined association patterns of FLT3 ITD and WT AMLs and found that FLT3-ITD signaling is associated with common gene expression and chromatin signature. Examination of genome-wide DNaseI hypersensitivite sites in FLT3 ITD and WT AML.

2015-07-03 | E-GEOD-64864 | biostudies-arrayexpress

Genome-wide Dnase-Seq profiles in Hodgkin's and non-Hodgkin's lymphoma

Project description:We report corresponding gene expression, promoter methylation patterns of differential DHSs as well as differentially occupied TF binding motifs using surrounding DNAseI cut profiles. Overall, our study provides a framework for model studies of HL and NHL pathologies. Examination of genome-wide DNaseI hypersensitive sites in L1236, L428, L591, Reh and Namalwa cell lines.

2014-09-24 | E-GEOD-51726 | biostudies-arrayexpress

Transcriptional landscape of Rag2 -/- thymocytes [Mnase-Seq]

Project description:We performed ChIP-Seq for hallmark TFs (Ets1, Runx1), histone modification marks (H3K4me1, H3K4me2, H3K4me3, H3K27me3, H3K36me3), total RNA Pol II, short RNA-Seq as well as nucleosome mapping mainly in murine Rag2 -/- thymocytes. We also performed ChIP-Seq for E47 as well as nucleosome mapping, gene expression microarray analysis in CD4+ CD8+ DP thymocytes. Overall, we find a key role for the transcription factor Ets1, contributing towards alpha beta T cell lineage commitment via differential transactivation of stage-specific genes orchestrated by dynamic, co-association -mediated chromatin remodeling, as well as transcription dependent generation of a specialized chromatin structure at the TCR beta locus. Genome-wide analysis via ChIP-Seq for Ets1, Runx1, total RNA Pol II binding, H3K4me1, H3K4me2, H3K4me3, H3K27me3, H3K36me3, short RNA-Seq, Mnase-Seq in murine Rag2 -/- thymocytes, ChIP-Seq for E47, Mnase-Seq and gene expression microarray analysis in DP thymocytes This Series represents Mnase-Seq data.

2014-04-01 | E-GEOD-56360 | biostudies-arrayexpress

Effect of Ets1 knockdown in the P5424 thymic cell line

Project description:We performed ChIP-Seq for Ets1 and histone modifications in P5424 thymic cells, without and with Ets1 knockdown via shRNA. Overall, we find that loss of Ets1 results in specific, higher occupancy of H3K4me1-marked nucleosomes at the Ets1 binding site, but not H3K4me3 nucleosomes. We verified the specificity of this mechanism as Ets1-dependent by also computing H3K4me1 and 3 nucleosome occupancy in hypersensitive, Ets1-depleted sites. This effect was also found in primary WT DN+DP Ets1 sites. Overall, this suggests that Ets1 induces chromatin remodeling and that its loss increases H3K4me1 nucleosome occupancy in bound sites, with levels of H3K4me3 comparatively unchanged, thus reducing the activation status of these enhancers Genome-wide analysis via ChIP-Seq for Ets1, H3K4me1 and H3K4me3 in WT, sh-scramble and sh-Ets1 the P5424 thymic cell line

2015-12-19 | E-GEOD-74042 | biostudies-arrayexpress

Transcriptional landscape of Rag2 -/- thymocytes [ChIP-Seq]

2014-04-01 | E-GEOD-56393 | biostudies-arrayexpress

Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [Agilent]

Project description:We performed genome-wide DNaseI hypersensitive site in FLT3-ITD and WT patient samples. We report corresponding gene expression, promoter methylation patterns of differential DHSs as well as differentially occupied TF binding motifs using surrounding DNAseI cut profiles. We examined association patterns of FLT3 ITD and WT AMLs and found that FLT3-ITD signaling is associated with common gene expression and chromatin signature. Examination of gene expression patterns in FLT3 ITD and WT AML via microarray study.

2015-07-03 | E-GEOD-64873 | biostudies-arrayexpress

Chronic growth factor signaling in Acute Myeloid Leukemia is connected to a specific chromatin signature [Methylation]

Project description:We performed genome-wide DNaseI hypersensitive site in FLT3-ITD and WT patient samples. We report corresponding gene expression, promoter methylation patterns of differential DHSs as well as differentially occupied TF binding motifs using surrounding DNAseI cut profiles. We examined association patterns of FLT3 ITD and WT AMLs and found that FLT3-ITD signaling is associated with common gene expression and chromatin signature. Examination of DNA methylation patterns in FLT3 ITD and WT AML via microarray study.

2015-07-03 | E-GEOD-64934 | biostudies-arrayexpress

Splicing enhances recruitment of methyltransferase HYPB/Setd2 and methylation of histone H3 lysine 36

Project description:Several lines of recent evidence support a role for chromatin in splicing regulation. Here we show that splicing can also contribute to histone modification, which implies a bidirectional communication between epigenetics and RNA processing. Genome-wide analysis of histone methylation in human cell lines and mouse primary T cells reveals that intron-containing genes are preferentially marked with H3K36me3 relative to intronless genes. In intron-containing genes, H3K36me3 marking is proportional to transcriptional activity, whereas in intronless genes H3K36me3 is always detected at much lower levels. Furthermore, splicing inhibition impairs recruitment of H3K36 methyltransferase HYPB/Setd2 and reduces H3K36me3, whereas splicing activation has the opposite effect. Moreover, the increase of H3K36me3 correlates with the length of the first intron, consistent with the view that splicing enhances H3 methylation. We propose that splicing is mechanistically coupled to recruitment of HYPB/Setd2 to elongating RNA Polymerase II. This experiment proposes to profile genome-wide binding profiles by ChIP-seq (Illumina, 36 bp tags) of RNA polymerase II (one biological replicate), the histone modification H3K36me3 (2 replicates) and a reference control input sample (genomic DNA after reverse cross-link, one replicate) in a human H1299 lung carcinoma cell line *** Raw data not provided for Samples GSM766322-GSM766324.

2011-07-25 | E-GEOD-30902 | biostudies-arrayexpress

ChIP-seq of CIC (Capicua) and histone marks (H3K9ac, H3K27ac and H3K4me1) in glioma neural stem cells (GNS) G144, human foetal neural stem cells (hNSC) and mouse embryonic stem cells (mESC),

Project description:We identified genome-wide binding patterns of CIC in several different cell types and find that CIC target genes are enriched for MAPK effector genes involved in cell cycle regulation and proliferation. CIC binding to its target genes is abolished by high MAPK activity, which leads to hyperacetylation and their transcriptional activation. Inhibition of MAPK signaling via MEK inhibition leads to recruitment of CIC to its target genes. Expression data of G144 cells after MEK inhibition and CIC knockout is available under accession E-MTAB-6681

2018-05-31 | E-MTAB-6682 | biostudies-arrayexpress

GRP94 rewires and buffers the FLT3-ITD signaling network and promotes survival of acute myeloid leukemic stem cells

Project description:Internal tandem duplications in the tyrosine kinase receptor FLT3 (FLT3-ITD) are among the most common lesions in acute myeloid leukemia (AML) and there exists a need for new forms of treatment. Using ex vivo drug sensitivity screening, we found that FLT3-ITD+ patient cells are particularly sensitive to HSP90 inhibitors. While it is well known that HSP90 is important for FLT3-ITD stability, we found that HSP90 family members play a much more complex role in FLT3-ITD signaling than previously appreciated. First, we found that FLT3-ITD activates the unfolded protein response (UPR), leading to increased expression of GRP94/HSP90B1. GRP94 rewires FLT3-ITD signaling by binding and retaining FLT3-ITD in the ER, where it aberrantly activates downstream signaling pathways. Second, HSP90 family proteins protect FLT3-ITD+ AML cells against apoptosis by alleviating proteotoxic stress, and treatment with HSP90 inhibitors results in proteotoxic overload that triggers UPR-induced apoptosis. Importantly, leukemic stem cells are strongly dependent upon HSP90 for their survival, and the HSP90 inhibitor ganetespib causes leukemic stem cell exhaustion in mouse PDX models. Taken together, our study reveals a molecular basis for HSP90 addiction of FLT3-ITD+ AML cells and provides a rationale for including HSP90 inhibitors in the treatment regime for FLT3-ITD+ AML.

2020-09-02 | PXD009423 | Pride

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