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ChIP-sequencing to investigate occupancy of wild-type and fusion ZNF384 proteins in murine pre-B cells

ABSTRACT: ChIP-sequencing to investigate occupancy of wild-type and fusion ZNF384 proteins in murine pre-B cells

PROVIDER: PRJNA448180 | ENA |

REPOSITORIES: ENA

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ChIP-sequencing to investigate occupancy of wild-type and fusion ZNF384 proteins in murine pre-B cells

Project description:We report the changes in chromatin occupancy between HA-tagged wild-type ZNF384 and the two leukemogenic fusion proteins, TAF15-ZNF384, and TCF3-ZNF384, in Arf-/- pre-B cells. Using ChIP-sequencing we found that 2298 peaks have new or increased binding while 495 peaks have decreased or lost binding of the fusion proteins compared to wild-type ZNF384.

2018-10-18 | GSE112560 | GEO

RNA-sequencing to investigate transcriptional changes caused by ZNF384 fusion proteins in murine pre-B cells

Project description:RNA-sequencing to investigate transcriptional changes caused by ZNF384 fusion proteins in murine pre-B cells

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RNA-sequencing to investigate transcriptional changes caused by ZNF384 fusion proteins in murine pre-B cells

Project description:RNA-sequencing was performed on Arf-/- pre-B cell expressing either wild-type ZNF384, TAF15-ZNF384, or TCF3-ZNF384. We found that pre-B cells that express ZNF384 fusion proteins have a gene expression profile similar to patients with ZNF384-rearranged leukemia.

2018-10-18 | GSE112558 | GEO

iCLIP of GFP fusion proteins

Project description:iCLIP of GFP fusion proteins

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Fusion partner directed chromatin occupancy drives the transcriptome heterogeneity of MLL-fusion acute lymphoblastic leukemia

Project description:Fusion of the N-terminus of the mixed-lineage-leukemia (MLL) gene with various partner genes drives acute lymphoblastic leukemia (ALL). Despite the fusion proteins sharing some common attributes, transcriptome heterogeneity of MLL-fusion ALL is observed and the underlying mechanism and biological consequences are unknown. We compared the genome-wide occupancy of MLL-Af4 and MLL-AF9 in human ALL cells expressing FLAG-tagged fusion proteins. Although both oncoproteins retain the same MLL N-terminal domains that mediate chromatin binding, the two fusion proteins displayed largely non-overlapping binding profiles, with MLL-AF9 showing preferential binding at repetitive elements. The binding specificity of each fusion protein was associated with differential global gene activation distinguishing the two ALLs. A subset of prednisolone response genes were among the differentially regulated targets, and the resistance related genes were specifically upregulated in MLL-Af4/AF4 cells. These studies provide evidence that distinct chromatin occupancy of different MLL-fusion proteins is one driving force for transcriptome heterogeneity of MLL-fusion ALL, which could potentially result in the disparate therapeutic outcome of the disease.

2018-04-30 | GSE103947 | GEO

Changes in gene expression over time in cells expressing t(4;11) fusion proteins

Project description:We have used a constitutive MLL-AF4 fusion gene together with a inducible AF4-MLL fusion gene to investigate the power of theses fusion proteins. All transgenes were stably or transiently transfected.

2021-06-19 | GSE178465 | GEO

Changes in chromatin accessibility over time in cells expressing t(4;11) fusion proteins [I]

2021-06-22 | GSE178567 | GEO

Fusion partner directed chromatin occupancy drives the transcriptome heterogeneity of MLL-fusion acute lymphoblastic leukemia

Project description:Fusion partner directed chromatin occupancy drives the transcriptome heterogeneity of MLL-fusion acute lymphoblastic leukemia

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Nuclear Condensation of NUP98-Fusion Proteins drives leukemogenic gene expression

Project description:NUP98-fusion proteins cause acute myeloid leukemia via unknown molecular mechanisms. All NUP98-fusion proteins share an intrinsically disordered region (IDR) featuring >35 repeats of Phenylalanine-Glycine (FG) in the NUP98 N-terminus. Conversely, different C-terminal NUP98-fusion partners are often transcriptional and epigenetic regulators. Given these structural features we hypothesized that mechanisms of oncogenic transformation by NUP98-fusion proteins are hard-wired in their protein interactomes. Affinity purification coupled to mass spectrometry of five distinct NUP98-fusion proteins revealed a conserved set of interactors that was highly enriched for proteins involved in biomolecular condensation. We developed biotinylated isoxazole-mediated condensome mass spectrometry (biCon-MS) to show that NUP98-fusion proteins alter the global composition of biomolecular condensates. In addition, an artificial FG-repeat containing fusion protein was able to phenocopy the induction of leukemic gene expression as mediated by NUP98-KDM5A. Thus, we propose that IDR-containing fusion proteins have evolved to uniquely combine biomolecular condensation with gene control to induce cancer.

2021-02-16 | GSE159037 | GEO

Menin-MLL inhibitors block oncogenic transformation by MLL fusion proteins in a fusion partner independent manner

Project description:Chromosomal rearrangements of the Mixed Lineage Leukemia (MLL) gene result in fusion proteins which retain the N-terminal portion of MLL fused with one of more than 70 different fusion partners. The high diversity of MLL fusion partners raises a question whether it is possible to develop a general therapeutic strategy to block the oncogenic activity of MLL fusion proteins in a fusion partner independent manner. We have demonstrated that blocking the menin-MLL interaction using small molecule inhibitor inhibits oncogenic activity of different MLL fusion proteins according to a mechanism that is independent on the fusion partner.

2018-06-09 | GSE69740 | GEO

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