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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.

2019-06-10 | GSE123401 | GEO

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)

2014-10-16 | E-GEOD-62302 | biostudies-arrayexpress

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

Project description:Either loss of EZH2 or redcuction of let-7 induces expression of HMGA2 and provokes severe myelofibrosis in mice carrying JAK2V617F. Therefore we compared gene expression profiles of LSK cells among WT mice, Hmga2-Tg mice, JAK2V617F-Tg mice, JAK2V617F/Hmga2 double-Tg mice, and JAK2V617F-Tg/EZH2 conditional KO mice.

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

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

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

2014-10-16 | GSE62302 | GEO

Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm

Project description:The somatic JAK2V617F mutation is found in a majority of patients with myeloproliferative neoplasms (MPN). Chronic inflammation is often associated with MPN, but the role of inflammation in the pathogenesis of MPN remains elusive. Expression of interleukin-1 (IL-1), a key regulator of inflammation, is found elevated in MPN. Here, we show that increased IL-1β enhances myeloid cell expansion and promotes the development of bone marrow (BM) fibrosis in heterozygous Jak2V617F mouse model of MPN. Genetic deletion of IL-1 receptor 1 (IL-1R1) preferentially inhibited the expansion of Jak2 mutant hematopoietic stem/progenitor cells. Furthermore, IL-1R1 deletion or blockade with anti-IL-1R1 antibody significantly reduced leukocytosis and splenomegaly, and markedly inhibited BM fibrosis in homozygous Jak2V617F mutant mice. Collectively, our results suggest that IL-1 signaling plays an important role in progression to BM fibrosis in MPN, and targeting of IL-1R1 could be a useful strategy for the treatment of myelofibrosis.

2022-08-05 | GSE180339 | GEO

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

Project description:V617F driver mutation of JAK2 is the leading cause of the Philadelphia-chromosome-negative myeloproliferative neoplasms (MPNs). Loss of Plek2 ameliorated JAK2V617F-induced myeloproliferative phenotypes including erythrocytosis, neutrophilia, thrombocytosis, and splenomegaly, thereby reverting the widespread vascular occlusions and lethality of JAK2V617F knockin mice. To reveal the role of Plek2 in the pathogenesis of JAK2V617F-induced MPNs and the detail mechanisms of its rescue, we performed RNA sequencing to analyze the gene expression profiles change between JAK2V617F/+ Plek2+/+ and JAK2V617F/+ Plek2-/- erythroblasts and hematopoietic stem/progenitor cells.

2019-04-11 | GSE97658 | GEO

Jak2V617F Reversible Activation Shows an Essential Requirement for Jak2V617F in Myeloproliferative Neoplasms

Project description:Janus kinases (JAKs) mediate cytokine signaling, cell growth and hematopoietic differentiation. Gain-of-function mutations activating JAK2 signaling are seen in the majority of myeloproliferative neoplasm (MPN) patients, most commonly due to the JAK2V617F driver allele. While clinically-approved JAK inhibitors improve symptoms and outcomes in MPNs, remissions are rare, and mutant allele burden does not substantively change with chronic JAK inhibitor therapy in most patients. This has been postulated to be due to incomplete dependence on constitutive JAK/STAT signaling, alternative signaling pathways, and/or the presence of cooperating disease alleles; however we hypothesize this is due to the inability of current JAK inhibitors to potently and specifically abrogate mutant JAK2 signaling. We therefore developed a conditionally inducible mouse model allowing for sequential activation, and then inactivation, of Jak2V617F from its endogenous locus using a Dre-rox/Cre-lox dual orthogonal recombinase system. Deletion of oncogenic Jak2V617F abrogates the MPN disease phenotype, induces mutant-specific cell loss including in hematopoietic stem/progenitor cells, and extends overall survival to an extent not observed with pharmacologic JAK inhibition. Furthermore, reversal of Jak2V617F in MPN cells with antecedent loss of Tet2 abrogates the MPN phenotype and inhibits mutant stem cell persistence suggesting cooperating epigenetic-modifying alleles do not alter dependence on mutant JAK/STAT signaling. Our results suggest that mutant-specific inhibition of JAK2V617F represents the best therapeutic approach for JAK2V617F-mutant MPN and demonstrate the therapeutic relevance of a dual-recombinase system to assess mutant-specific oncogenic dependencies in vivo.

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Jak2 mediated phosphorylation and activation of TET2 in hematopoiesis

Project description:FDCP cells were stably transfected with JAK2V617F or WT JAK2 vectors and then examined for genome wide methylation with the HELP assay

2020-01-01 | GSE116537 | GEO

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