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Whole-genome CRISPR screening identifies N-glycosylation as an essential pathway and a potential novel therapeutic target in CALR-mutant MPN (RNA-Seq).

ABSTRACT: Whole-genome CRISPR screening identifies N-glycosylation as an essential pathway and a potential novel therapeutic target in CALR-mutant MPN (RNA-Seq).

PROVIDER: PRJNA840898 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19332582_1.fastq.gz	Fastqsanger.gz
	SRR19332582_2.fastq.gz	Fastqsanger.gz
	SRR19332583_1.fastq.gz	Fastqsanger.gz
	SRR19332583_2.fastq.gz	Fastqsanger.gz
	SRR19332584_1.fastq.gz	Fastqsanger.gz

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Whole-genome CRISPR screening identifies N-glycosylation as an essential pathway and a potential novel therapeutic target in CALR-mutant MPN (Pooled CRISPR Screen).

Project description:Calreticulin (CALR) mutations are frequent, disease-initiating events in myeloproliferative neoplasms (MPN). Although the biological mechanism by which CALR mutations cause MPN has been elucidated, there currently are no clonally selective therapies for CALR-mutant MPN. To identify unique genetic dependencies in CALR-mutant MPN, we performed a whole-genome CRISPR knockout depletion screen in mutant CALR-transformed hematopoietic cells. We found that genes in the N-glycosylation pathway (amongst others) were differentially depleted in mutant CALR-transformed cells as compared with control cells. Using a focused pharmacological screen targeting unique vulnerabilities uncovered in the CRISPR screen, we found that chemical inhibition of N-glycosylation impaired the growth of mutant CALR-transformed cells in vitro. We treated Calr-mutant knockin mice with the N-glycosylation inhibitor, 2-deoxy-glucose (2-DG), and found a preferential sensitivity of Calr-mutant cells to 2-DG as compared to wild-type cells, and a normalization of key MPN disease features. These findings advance the development of clonally selective treatments for CALR-mutant MPN.

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Whole-genome CRISPR screening identifies N-glycosylation as an essential pathway and a potential novel therapeutic target in CALR-mutant MPN (Whole Genome CRISPR Screen).

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Whole-genome CRISPR screening identifies N-glycosylation as an essential pathway and a potential novel therapeutic target in CALR-mutant MPN

Project description:Whole-genome CRISPR screening identifies N-glycosylation as an essential pathway and a potential novel therapeutic target in CALR-mutant MPN

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Gene expression data from CD34+ BMMCs/PBMCs from JAK2V617F positive and CALR mutated MPN patients

Project description:Philadelphia chromosome-negative myeloproliferative neoplasms (MPN) consist of primary myelofibrosis (PMF), polycythemia vera (PV), essential thrombocythemia (ET) In this dataset, we compare the gene expression data of patients JAK2V617F vs. CALR-mutated MPN patients.

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Whole-genome CRISPR screening identifies N-glycosylation as an essential pathway and a potential novel therapeutic target in CALR-mutant MPN (Pooled CRISPR Screen).

Project description:Whole-genome CRISPR screening identifies N-glycosylation as an essential pathway and a potential novel therapeutic target in CALR-mutant MPN (Pooled CRISPR Screen).

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Whole-genome CRISPR screening identifies N-glycosylation as an essential pathway and a potential novel therapeutic target in CALR-mutant MPN (Whole Genome CRISPR Screen).

Project description:Whole-genome CRISPR screening identifies N-glycosylation as an essential pathway and a potential novel therapeutic target in CALR-mutant MPN (Whole Genome CRISPR Screen).

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RNA seq of natural killer (NK) cells of MPN patients with mutations in calreticulin (CALR) and healthy controls

Project description:To assess the transcriptional differences between natural killer (NK) cells from patients with myeloproliferative neoplasms (MPN) carrying a mutation in calreticulin (CALR) and healthy donors (HD), bulk RNA sequencing was performed. Peripheral blood mononuclear cells (PBMC) were isolated from the blood of 4 HD and 4 CALR-mutant MPN patients using Ficoll density gradient and were cryopreserved after the isolation process. CD45+SSClowCD3-CD56+ cells were sorted from cryopreserved PBMC samples and RNA was isolated.

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Project description:Mutant ASXL1 exacerbates CALR-mutant MPN by enhancing a distinct megakaryocyte differentiation program

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Mutant ASXL1 exacerbates CALR-mutant MPN by enhancing a distinct megakaryocyte differentiation program [Patient scRNA-seq]

Project description:Mutant ASXL1 exacerbates CALR-mutant MPN by enhancing a distinct megakaryocyte differentiation program

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Mutant ASXL1 exacerbates CALR-mutant MPN by enhancing a distinct megakaryocyte differentiation program [murine scRNA-seq]

Project description:Mutant ASXL1 exacerbates CALR-mutant MPN by enhancing a distinct megakaryocyte differentiation program

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