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Gene expression profile of mock and FLT3-ITD-expressing K562 cells.

ABSTRACT: We used whole genome microarray expression profiling as a discovery platform to identify genes regulated by FLT3-ITD activity.

ORGANISM(S): Homo sapiens

PROVIDER: GSE64330 | GEO | 2015/09/09

SECONDARY ACCESSION(S): PRJNA270753

REPOSITORIES: GEO

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Gene expression profile of mock and FLT3-ITD-expressing K562 cells.

Project description:We used whole genome microarray expression profiling as a discovery platform to identify genes regulated by FLT3-ITD activity. Viral particles with pMY-puro, pMY-puro-FLT3-ITD-1 or pMY-puro-FLT3-ITD-2, were generated using PLAT-gp packaging cells and infected to K562 cells. The vector-transduced cells were selected with 2µg/ml puromycin treatment.

2015-09-09 | E-GEOD-64330 | biostudies-arrayexpress

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Project description:The miR-155-dependent differences in gene expression in the HSPC compartment of FLT3-ITD mice is unknown. In this experiment, we performed RNA sequencing on FLT3-ITD and FLT3-ITD miR-155-/- mouse LKS cells.

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MS-based phosphoproteomic of cytarabine-treated FLT3-ITD cells

Project description:ITD mutations in the FLT3 gene occur in the 30% of acute myeloid leukemia patients. The integration of ITD in the tyrosine kinase domain (TKD-ITD) of the FLT3 receptor has been shown to confer resistance to standard chemotherapy treatment. We applied state-of-the-art, high-sensitive, mass spectrometry (MS)-based (phospho)proteomics to investigate the molecular mechanisms underlying the sensitivity to cytarabine therapy in FLT3-ITD cells.

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CircMYBL2 Regulates FLT3-ITD FLT3AML Translation in AML

Project description:CircMYBL2 is more highly expressed in AML patients with FLT3-ITD mutations than in those without the FLT3-ITD mutation. We found that circMYBL2 knockdown specifically inhibits proliferation and promotes the differentiation of FLT3-ITD AML cells in vitro and in vivo. We used the ribosome profiling and RNA-seq libraries sequenced with Illumina HiSeq 2500 to identify the mRNA that circMYBL2 targeted. Interestingly, we found that circMYBL2 significantly influences the protein level of mutant FLT3 kinase, which contributes to the activation of FLT3-ITD-dependent signaling pathways. Mechanistically, circMYBL2 enhanced the translational efficiency of FLT3 kinase by increasing the binding of PTBP1 to FLT3 mRNA. Moreover, circMYBL2 knockdown impaired the cytoactivity of inhibitor-resistant FLT3-ITD-positive cells, with a significant decrease in FLT3 kinase expression, followed by the inactivation of its downstream pathways. In summary, we are the first to reveal a circRNA that specifically influences FLT3-ITD AML and regulates FLT3 kinase levels through translational regulation, suggesting that circMYBL2 may be a potential therapeutic target for FLT3-ITD AML.

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PRMT1-mediated FLT3 arginine methylation promotes FLT3-ITD+ Acute Myeloid Leukemia maintenance

Project description:We want to obtain FLT3-ITD gene signature. To do so, we transduced CB CD34+ cells with mock or FLT3-ITD vectors and performed RNA sequencing (RNA-Seq). Two Groups: Group1: CB CD34+ cells transduced with mock vector; Group2: CB CD34+ cells transduced with FLT3-ITD vector;

2020-04-01 | GSE129754 | GEO

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2021-11-10 | GSE122435 | GEO

Enhancer chromatin marks in Dnmt3aKO/FLT3-ITD lymphoid leukemia

Project description:We mapped H3K4me1 and H3K27ac chromatin marks in Dnmt3aKO/FLT3-ITD and FLT3-ITD lymphoid leukemias

2016-05-19 | GSE80723 | GEO

identifying mRNA expression regulated by FLT3/ITD and Cxcl12

Project description:mRNA expression regulated by FLT3/ITD and Cxcl12 were compared in the Ba/F3 cells expressing wild type FLT3 or FLT3/ITD and incubated with or without Cxcl12.

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