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Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_DMSO_AC220_24hr]

ABSTRACT: Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_DMSO_AC220_24hr]

PROVIDER: PRJNA688229 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13313387.fastq.gz	Fastqsanger.gz
	SRR13313388.fastq.gz	Fastqsanger.gz
	SRR13313389.fastq.gz	Fastqsanger.gz
	SRR13313390.fastq.gz	Fastqsanger.gz
	SRR13313391.fastq.gz	Fastqsanger.gz

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Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia

Project description:Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia

| PRJNA688227 | ENA

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VIVO]

Project description:Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VIVO]

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Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VITRO]

Project description:Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VITRO]

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Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_ATF4_RNAP2_CHIP]

Project description:Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_ATF4_RNAP2_CHIP]

| PRJNA688222 | ENA

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VIVO]

Project description:We performed 3'-RNA-Sequencing on RNA isolated from murine MLL-AF9/iFLT3-ITD cells where the inducible iFLT3-ITD transgene had been depleted for 48 hours compared to non-depleted conditions in vivo to perform differential gene expression analysis.

2021-01-13 | GSE163927 | GEO

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [iFLT3-ITD-Depletion_In VITRO]

Project description:We performed 3'-RNA-Sequencing on RNA isolated from murine MLL-AF9/iFLT3-ITD cells where the inducible iFLT3-ITD transgene had been depleted for 24 or 48 hours compared to non-depleted conditions in vitro to perform differential gene expression analysis.

2021-01-13 | GSE163926 | GEO

Expression profile of hematopoietic stem and progenitor cell (HSPC) compartment of FLT3-ITD and FLT3-ITD miR-155-/- mice

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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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.

2019-07-09 | GSE133925 | GEO

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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.

2023-07-20 | PXD038638 | Pride

Serine biosynthesis is a metabolic vulnerability in FLT3-ITD-driven acute myeloid leukaemia [MV411_OCI-AML3_DMSO_AC220_24hr]

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2021-01-13 | GSE163930 | GEO

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