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RNA-seq data from VavCre Jak2+/+ Cdk6+/+, VavCre Jak2V617F Cdk6+/+, VavCre Jak2V617F Cdk6-/-, VavCre Jak2+/+ Cdk6-/- murine bone marrow LSK cells and VavCre Jak2V617F Cdk6+/+ Palbociclib treated murine bone marrow LSK cells

ABSTRACT: RNA-seq data from VavCre Jak2+/+ Cdk6+/+, VavCre Jak2V617F Cdk6+/+, VavCre Jak2V617F Cdk6-/-, VavCre Jak2+/+ Cdk6-/- murine bone marrow LSK cells and VavCre Jak2V617F Cdk6+/+ Palbociclib treated murine bone marrow LSK cells

PROVIDER: PRJNA508629 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8284740.fastq.gz	Fastqsanger.gz
	SRR8284741.fastq.gz	Fastqsanger.gz
	SRR8284742.fastq.gz	Fastqsanger.gz
	SRR8284743.fastq.gz	Fastqsanger.gz
	SRR8284744.fastq.gz	Fastqsanger.gz

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RNA-seq data from VavCre;Jak2+/+; Cdk6+/+, VavCre;Jak2V617F; Cdk6+/+, VavCre;Jak2V617F; Cdk6-/-, VavCre; Jak2+/+; Cdk6-/- murine bone marrow LSK cells and VavCre; Jak2V617F; Cdk6+/+ Palbociclib treated murine bone marrow LSK cells

Project description:We describe a critical role for Cdk6 in JAK2V617F+ MPN evolution. The absence of Cdk6 ameliorates clinical symptoms and prolongs survival of JAK2V617F fl/+ vav-Cre mice. The Cdk6 protein interferes with three hallmarks of disease: besides regulating malignant stem cell quiescence, it promotes NFkB signaling and contributes to cytokine production while inhibiting apoptosis. The treatment with palbociclib did not mirror these effects, showing that the functions of Cdk6 in MPN pathogenesis are largely kinase-independent.

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RNA sequencing of LSK cells from mice with JAK2 mutation and HMGA2 expression

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2017-06-01 | GSE87464 | GEO

Single cell RNA Seq to study the effects of kinase-inactivated Cdk6 or a Cdk6 knock-out in the mouse LSK cell compartment

Project description:To understand kinase-dependent and kinase-independent functions of Cdk6 in the hematopoietic stem and progenitor compartment, mouse models carrying wild-type Cdk6 (Cdk6_WT), a homozygous knock-in of a kinase-inactivated variant of Cdk6 (Cdk6_K43M) or a homozygous Cdk6 knock-out (Cdk6_KO) were used. From these mice, lineage-negative, Sca1-positive, c-Kit-positive cells (LSK cells) were isolated by means of flow cytometry cell sorting. 30000 LSK cells per mouse were subjected to library prep for single cell RNA Sequencing using the Chromium NextGem Single Cell 5’ v2 Kit (10x Genomics, Pleasanton, CA, USA)

2024-05-22 | E-MTAB-13149 | biostudies-arrayexpress

Expression data from loss-of-TET2 and/or JAK2V617F mutant Lineage-c-Kit+Sca-1+ (LSK) bone marrow cells

Project description:Recent studies have shown that both TET2 mutation and JAK2V617F mutation are frequent in myeloproliferative neoplasms patients. The pathophysiological roles of each mutation have been elucidated in murine models, but the cooperative effect of the two mutations has not been elucidated yet. In this study, we examined the function of the cooperative effect of loss-of-TET2 function and JAK2V617F mutation in murine hematopoiesis. In this study, we utilized wild type (WT) mice, TET2 knock down (TET2KD) mice, JAK2V617F transgenic mice, double mutant mice. We transplanted 4 types of E14.5 fetal liver cells (WT, TET2KD, JAK2V617F, double mutant) into lethally irradiated mice. At 10-16 weeks post-transplantation, LSK cells from the BM of the recipients were collected, and gene expression analysis was performed. (WT,5 mice at 16 weeks; TET2KD, 5 mice at 10 weeks; JAK2V617F, 5 mice at 16 weeks; double mutant, 5 mice at 13 weeks)

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JAK2V617F mutation in CD34+ stem cells of essential thrombocythemia

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JAK2V617F mutation in CD34+ stem cells of essential thrombocythemia

Project description:The JAK2V617F mutation has been reported in about 40-60% of Essential Thrombocythemia (ET) patients. However, little is known about specific molecular abnormalities of the hematopoietic stem cell compartment of ET according to JAK2 mutation. Therefore, we compared the gene expression profiles of bone marrow (BM) CD34+ cells from 16 patients with and without the JAK2V617F mutation to identify differentially expressed genes. Keywords: cell type comparison Sample name and JAK2V617F mutation: - BM CD34+ cells from healthy subject (CTR) - ET JAK2V617F-positive: ET 1, ET 4, ET 6, ET 7, ET 8, ET 10, ET 12, ET 15 - ET JAK2V617F-negative: ET 2, ET 3, ET 5, ET 9, ET 11, ET 13, ET 14, ET 16

2010-04-06 | E-GEOD-9827 | biostudies-arrayexpress

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Project description:Myelofibrosis (MF) is a deadly blood neoplasia that presents the worst prognosis among myeloproliferative neoplasms (MPN). Expression of CDK6 is significantly elevated in MPN/MF hematopoietic progenitor cells. In this study, we investigated the efficacy of CDK4/6 inhibitor Palbociclib alone or in combination with Ruxolitinib in Jak2V617F and MPLW515L murine models of MF. Treatment of Palbociclib alone significantly reduced leukocytosis, splenomegaly and inhibited bone marrow fibrosis in Jak2V617F and MPLW515L mouse models of MF. Combined treatment of Palbociclib and Ruxolitinib resulted in normalization of peripheral blood leukocyte counts, marked reduction of spleen size and abrogation of bone marrow fibrosis in murine models of MF. Mechanistically, we show that Palbociclib treatment or depletion of CDK6 inhibits Aurora kinase, NF-κB and TGF-β signaling pathways in Jak2V617F mutant hematopoietic cells. Overall, our data suggest that Palbociclib in combination with Ruxolitinib may have therapeutic potential for treatment of MF.

2021-11-05 | GSE173814 | GEO

JAK2V617F mutant HSC microarray

Project description:Mutant JAK2V617F is found in majority of patients with myeloproliferative neoplasm. While heterozygous JAK2V617F induced an ET-like phenotype, JAK2V617F homozygosity drives an severe PV-like phenotype in knock-in mice. HSCs from mice with homozygous JAK2V617F expression show impaired self-renewal in transplants. To understand the molecular mechanisms involved this HSC functional defect, microarray was performed on isolated LT-HSCs from mice expressing wildtype, heterozygous and homozygous expression of mutant JAK2.

2018-08-06 | E-MTAB-6878 | biostudies-arrayexpress

Gene expression profiling to study the transcriptional consequences of Jak2V617F expression and/or Tet2 loss in murine hematopoietic stem cells

Project description:To interrogate the molecular pathways disrupted by Jak2V617F expression and/or Tet2 loss, Lin-negative, Sca-1-positive, c-kit-positive (LSK) hematopoietic progenitor cells were isolated from bone marrow of wild-type, Jak2V617F, Tet2-null or Jak2V617F/Tet2-null animals (n= 2-4 mice per group) and subjected to gene expression profiling.

2014-10-31 | E-MTAB-2986 | biostudies-arrayexpress

Quantitative Analysis of JAK2V617F/+ Plek2+/+ and JAK2V617F/+ Plek2-/- erythroblast and hematopoietic stem cells/ progenitor cells Transcriptomes

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