Project description:Using ATAC-seq, we examined genome-wide chromatin accessibility in the MOLM13 and MV4;11 human MLL-fusion acute myeloid leukemia cell lines.
Project description:Purpose: Compare transcriptional changes between drug treated (gilteritinib, TP-0903) and vehicle in acute myeloid leukemia xenografts. Methods: FLT3-ITD+ MOLM13-RES-Luc+ (MOLM13 cells with a D835Y mutation generating a resistant phenotype) AML cells were xenografted into NSG mice. Mice were randomized according to bioluminescence imaging, and treatment of FLT3 tyrosine kinase inhibitor (gilteritinib, 30 mg/kg, once daily for 5 days/week) was started on day 13 post-tail vein injection. At study end point, mice were humanely euthanized and bone marrow was collected. AML cells (human CD45+) were isolated, and ATAC-seq was performed on HiSeq 4000, total RNA. Sequencing reads were aligned and analyzed for differential gene expression of treatment vs vehicle cohorts. Results: The analysis revealed the chromatin accessibility changes induced by gilteritinib in MOLM13-RES AML xenograft model.
Project description:We report the genome wide distribution of H3K79 dimethylation in the human MLL-AF6 rearranged cell line ML2 as well as the human MOLM13 and HL60 cell lines
Project description:We report the genome wide distribution of H3K79 dimethylation in the human MLL-AF6 rearranged cell line ML2 as well as the human MOLM13 and HL60 cell lines Examination of H3K79 dimethylation in the MLL-AF6 fusion positive human leukemia cell line ML2 and control cell lines MOLM-13 and HL60. The MLL-AF6 positive ML2 cell line (obtained from DSMZ) and the cell lines HL60 and MOLM 13 were grown under standard conditions and 1 million cells were fixed/crosslinked and used for ChIP-seq with H3K79 dimethylation specific antibody Ab3594 (Abcam)
Project description:We present a computational method for building a regulatory network from global phosphoproteomic and transcription profiling data. To recover the critical missing links between signaling events and transcriptional responses, we relate changes in chromatin accessibility to changes in expression and then uses these links to connect proteomic and transcriptome data. We applied our approach to integrate epigenomic, phosphoproteomic and transcriptome changes induced by the variant III mutation of the epidermal growth factor receptor (EGFRvIII) in a cell line model of glioblastoma multiforme (GBM). Genome-wide DNase I hypersensitivity followed by sequencing (DNase-Seq) to measure chromatin accessibility in a cell line derived from the U87MG glioblastoma cell line to express high level of EGFRvIII (U87H; 2 million copies of EGFRvIII per cell) and a control cell line expressing kinase dead EGFRvIII (U87DK; 2 million kinase dead EGFRvIII per cell). A prediction from the computational method, the transcriptional co-regulator p300, was experimentally validated by chromatin immunoprecipitation followed by sequencing (ChIP-Seq).
Project description:Using ChIP-seq we examined the chromatin occupancy of IKAROS, MENIN, MLL1 and MEIS1 in the MOLM13 and MV4;11 human MLL-fusion acute myeloid leukemia cell lines.
Project description:A multi-omics study examining chromatin accessibility, transcriptome, proteome and phosphorylation patterns in the HBB homozygous knockout of the HUDEP2 cell line (HBB-KO)
Project description:Molm13 AML cell line both control and MPI KO, treated with AC220 (quizartinib) and mannose at 24 and 72 hours after drug treatment. 2 reads and 2 repeats for each condition, 2 timepoints, 48 total files.
Project description:RNA-seq followed by digital gene expression analyses we assessed genes that change upon CRISPR-Cas9-mediated knockout of YBX1 in myeloid leukemia cells (MOLM13 cell line).
Project description:RNA-seq followed by digital gene expression analyses we assessed genes that change upon CRISPR-Cas9-mediated knockout of YBX1 in myeloid leukemia cells (MOLM13 cell line).