Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of JAK2V617F HSPC and endogenous HSPC from irradiated and non-irradiated legs of recipient mice transplanted with JAK2V617F hematopoietic cells

ABSTRACT: using transplantation of transgenic knock-in JAK2V617F hematopoietic cells into a single irradiated leg, we show development of Polycythemia Vera (PV) from a single anatomical site in immuno-competent mice. Mutant cells colonizing the non-irradiated leg efficiently induce PV. We compared transcriptomic profiles of sorted JAK2V617F HSPC and their reciprocal endogenous WT HSPC in the non-irradiated and irradiated legs from recipient mice transplanted with JAK2V617F hematopoietic cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE165902 | GEO | 2022/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome analysis of JAK2V617F HSPC and endogenous HSPC from irradiated and non-irradiated legs of recipient mice transplanted with JAK2V617F hematopoietic cells

Project description:Transcriptome analysis of JAK2V617F HSPC and endogenous HSPC from irradiated and non-irradiated legs of recipient mice transplanted with JAK2V617F hematopoietic cells

| PRJNA698571 | ENA

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

Transcriptome analysis of JAK2wt and JAK2V617F+ iPSCs and iPSC-derived CD34+ progenitor-enriched cultures, either inflammatory cytokines treated or untreated.

Project description:PV-patient specific and control healthy individual-derived iPSCs were upon differentiation for 9 days into CD34+ hematopoietic progenitors treated with IFNγ, TNFα and TGFβ1 or untreated and used for transcriptome analysis. This dataset shows presence of cell-autonomous and strong non-cell autonomous JAK2V617F-dependet inflammatory footprint at the transcriptome level.

2020-12-03 | E-MTAB-7693 | biostudies-arrayexpress

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

Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells

Project description:We report a Jak2V617F knock-in mouse myeloproliferative neoplasm (MPN) model resembling human polycythemia vera (PV). The MPN is serially transplantable and we demonstrate that the hematopoietic stem cell (HSC) compartment has the unique capacity for disease initiation but does not have a selective competitive advantage over wild type HSCs. In contrast, myeloid progenitor populations are expanded and skewed towards the erythroid lineage, but cannot transplant the disease. Treatment with a JAK2 kinase inhibitor ameliorated the MPN phenotype, but did not eliminate the disease-initiating population. These findings provide insights into the consequences of JAK2 activation on HSC differentiation and function and have the potential to inform therapeutic approaches to JAK2V617F positive MPN. LKS cells were isolated from wild type (n=4) and JAK2V617F mutant mice (n=4). RNA was extracted using Qiagen RNeasy Micro Kit according to manufacturers instruction and amplified using NUGEN amplification kit. cDNA was fragmented and biotinylated before hybridization onto Affymetrix Mouse Expression Array 430 2.0.

2010-05-28 | E-GEOD-21842 | biostudies-arrayexpress

Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells

2010-05-15 | GSE21842 | GEO

Transcriptional profiling of normal and JAK2V617F-positive erythroblasts of polycythemia vera and essential thrombocythemia

Project description:This experiment was designed to identify genes differentially expressed in association with the JAK2V617F mutation in polycythemia vera (PV) and essential thrombocythemia (ET). Peripheral blood was obtained from 20 ET and 16 PV patients and erythroid progenitors were grown in semi-solid methylcellulose media supplemented with 0.01 U/ml erythropoietin. Individual clones were plucked and genotyped for the presence of the JAK2V617F mutation, and up to 20 normal and mutant colonies were pooled from each patient, and subjected to expression profiling. In total, 72 expression profiling datasets were generated, representing paired samples of normal and mutant cells from 36 patients.

2011-11-22 | E-MTAB-384 | biostudies-arrayexpress

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.

2022-05-25 | GSE203464 | GEO

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.

2018-10-29 | GSE120362 | GEO

Expression data from Lineage-c-Kit+Sca-1+ (LSK) and megakaryocyte/erythroid progenitor (MEP) cells isolated from WT, Ezh2?/?, JAK2V617F, and JAK2V617F/Ezh2?/? mice

Project description:Loss-of-function mutations in EZH2 are associated with worse outcomes in patients with primary myelofibrosis (PMF). To understand how EZH2 insufficiency is involved in the pathogenesis of PMF, we generated mice compound for Ezh2 conditional deletion and a JAK2V617F transgene. The total bone marrow cells isolated from Cre-ERT2, Ezh2flox/flox;Cre-ERT2, JAK2V617F;Cre-ERT2 and JAK2V617F;Ezh2flox/flox;Cre-ERT2 mice were transplanted into lethally irradiated CD45.1+ wild-type recipient mice. As we deleted Ezh2 at four weeks post transplantation, we performed gene-expression analysis of LSKs and MEPs isolated from the recipient mice at 2 months post transplantation.

2015-06-04 | E-GEOD-69498 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data