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Effect of Menin cKO on MLL-AF9 transformed cells

ABSTRACT: Effect of Menin cKO on MLL-AF9 transformed cells

PROVIDER: PRJNA483761 | ENA |

REPOSITORIES: ENA

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Effect of Menin cKO on MLL-AF9 transformed cells

Project description:We determined the effect of conditional deletion of Menin in MLL-AF9 transformed leukemia cells

2018-08-01 | GSE117933 | GEO

Chromatin state changes induced by targeted degradation of MLL-AF9 are phenocopied by combined DOT1L and MENIN inhibition. [ChIP-Seq]

Project description:Using ChIP-seq we examined the occupancy changes of various histone marks and chromatin-bound proteins following accute MLL-AF9 degradation in MLL-AF9-HA-FKPB12 transformed human (HCB1) cells. We also examined occupancy changes of various chromatin-bound proteins in human MLL-AF9-HA-FKBP12 transformed cells (HCB1) and MOLM13 cells in response to DOT1L inhibition, Menin-MLL inhibition, and the combination of DOT1L and Menin-MLL inhibition.

2022-03-03 | GSE173599 | GEO

Chromatin state changes induced by targeted degradation of MLL-AF9 are phenocopied by combined DOT1L and MENIN inhibition. [RNA-Seq]

Project description:Using RNA-seq we examined the transcriptional changes following MLL-AF9 degradation in MLL-AF9-HA-FKPB12 transformed murine (BM2222) and human (HCB1) cells. We also examined transcriptional changes in human MLL-AF9-HA-FKBP12 transformed cells (HCB1) and MOLM13 cells in response to DOT1L inhibition, Menin-MLL inhibition, and the combination of DOT1L and Menin-MLL inhibition. Lastly we assessed gene expression in murine neutrophils isolated directly from mice.

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Eed inactivation in Cdkn2a-null MLL-AF9 transformed cells

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Gene expression changes upon Mof knockout in MLL-AF9 transformed murine LSKs

Project description:We report Illumina next generation RNA sequencing (RNAseq) of MLL-AF9 in vitro transformed murine LSKs upon genetic deletion of Mof. These gene expression data illustrate that Mof regulates the expression of genes involved in DNA damage response and chromatin stability in MLL-AF9 transformed cells.

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Chromatin state changes induced by targeted degradation of MLL-AF9 are phenocopied by combined DOT1L and MENIN inhibition [ATAC-seq]

Project description:Using ATAC-seq we examined changes in chromatin accessibility following MLL-AF9 degradation in MLL-AF9-HA-FKBP12 transformed hCD34+ cells (HCB1) after 180 minutes.

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Chromatin state changes induced by targeted degradation of MLL-AF9 are phenocopied by combined DOT1L and MENIN inhibition. [SLAM-Seq]

Project description:Using SLAM-seq we examined the nascent transcriptional changes following MLL-AF9 degradation in MLL-AF9-HA-FKBP12 transformed hCD34+ cells (HCB1) after 15, 30, 60, and 120 minutes

2022-03-03 | GSE173571 | GEO

Chromatin state changes induced by targeted degradation of MLL-AF9 are phenocopied by combined DOT1L and MENIN inhibition [PRO-seq]

Project description:Using PRO-seq we examined nascent transcriptional changes and RNA Pol II pausing following MLL-AF9 degradation in MLL-AF9-HA-FKBP12 transformed hCD34+ cells (HCB1) after 15, 30, and 180 minutes

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Notch Pathway Activation Targets AML Cell Homeostasis and Differentiation: MLL-AF9 transformed LGMP

Project description:To determine role of Notch signaling in AML leukemia initiating cells we used a conditional mouse knock-in model of Notch1-IC to induce Notch1-IC expression in MLL-AF9 transformed LGMP. WT and Notch1-IC+ LGMP were analyzed to determined genes controlled by Notch signaling. 12 weeks old wt lethaly irradiated mice were transplanted with 50000 cKit+ MLL-AF9-IRES-YFP infected cells from MLL-AF9 EF1 wt/wt ROSAwt/CreERT2 or MLL-AF9 EF1 wt/lsl-N1-IC ROSAwt/CreERT2 mice + 250000 support wt total bone marrow cells. 4 weeks after transplant mice were injected 2 times with tamoxifen (0.2mg/g body weight) every other day. Mice were sacrificed and analyzed 6 days after last injection. LGMP were flow purified for RNA extraction and hybridization on Affymetrix microarrays.

2013-01-18 | E-GEOD-42260 | biostudies-arrayexpress

A novel Menin-MLL inhibitor induces specific chromatin changes and eradicates disease in models of MLL-rearranged leukemia [ChIP-seq]

Project description:Treatment of cells carrying MLL-rearrangements with VTP-50469 (specific Menin-MLL1 inhibitor) displaces Menin from high molecular weight complexes and chromatin genome-wide. Since VTP-50469 block Menin interaction with MLL1 we tested using chip-seq if treatment with VTP-50469 also displaces MLL1 or MLL-fusions from chromatin. We found that the VTP-50469 treatment displaced MLL-fusions from only a subset of MLL-fusion binding sites. Since DOT1L is associated with MLL-AF9 we then tested if displacement of MLL1 also leads to loss of DOT1L association with chromatin on MLL-AF9 binding sites. We found that DOT1L binds to thousands of genes, treatment with VTP-50469 leads to genome wide loss of DOT1L binding including the same subset of MLL-fusion binding sites.

2019-11-06 | GSE127507 | GEO

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