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Enforced Expression of NUP98-HOXA10hd Fusion Gene in Multipotent Progenitors Support Long-term Hematopoiesis in primary mice [MPP]

ABSTRACT: Enforced Expression of NUP98-HOXA10hd Fusion Gene in Multipotent Progenitors Support Long-term Hematopoiesis in primary mice [MPP]

PROVIDER: PRJNA611951 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11287647_1.fastq.gz	Fastqsanger.gz
	SRR11287647_2.fastq.gz	Fastqsanger.gz
	SRR11287648_1.fastq.gz	Fastqsanger.gz
	SRR11287648_2.fastq.gz	Fastqsanger.gz
	SRR11287649_1.fastq.gz	Fastqsanger.gz

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1 - 5 of 16

Similar Datasets

Enforced Expression of NUP98-HOXA10hd Fusion Gene in Multipotent Progenitors Support Long-term Hematopoiesis in primary mice [MPP]

Project description:Allogenic hematopoietic stem cell (HSC) transplantation is widely used for treatment of blood disorders to re-establish long-term multi-lineage hematopoiesis. Enhance self-renewal potential of progenitor population to support hematopoiesis offer an alternative and complementary approach to achieve similar or enhance therapeutic effects. Nup98-Hoxa10hd fusion gene (NA) has been shown to confer expansion, anti-stress response and engraftment competitiveness on HSC. However, whether the ectopic expression of NA in multipotent progenitors (MPPs) could enhance their self-renewal potential and confer long-term multi-lineage hematopoiesis remains unknown. In this study, we showed that ectopic expression in MPPs confer long-term multi-lineage hematopoiesis in recipient mice. We further showed that NA upregulated pathways of cell cycle regulation, epigenetic regulation and response to stress in MPPs. These molecular traits increased the self-renewal potential of NA MPPs, which resulting in production of lineage-maintaining committed progenitor cells. Transcriptome analysis of NA myeloid progenitors identified genes regulating hematopoiesis, homeostasis, phosphorylation. In summary, we show that ectopic expression of Nup98-Hoxa10hd fusion gene enhance self-renewal potential of MPPs thus confer long-term multi-lineage repopulating capacity on MPPs, offering promising means to involve MPPs to augment cell source in clinical transplantation settings.

2020-10-06 | GSE146780 | GEO

Enforced Expression of NUP98-HOXA10hd Fusion Gene in Multipotent Progenitors Support Long-term Hematopoiesis in primary mice

Project description:Enforced Expression of NUP98-HOXA10hd Fusion Gene in Multipotent Progenitors Support Long-term Hematopoiesis in primary mice

| PRJNA611950 | ENA

Enforced Expression of NUP98-HOXA10hd Fusion Gene in Multipotent Progenitors Support Long-term Hematopoiesis in primary mice [MP]

Project description:Enforced Expression of NUP98-HOXA10hd Fusion Gene in Multipotent Progenitors Support Long-term Hematopoiesis in primary mice [MP]

| PRJNA611952 | ENA

Enforced Expression of NUP98-HOXA10hd Fusion Gene in Multipotent Progenitors Support Long-term Hematopoiesis in primary mice [MP]

Project description:Allogenic hematopoietic stem cell (HSC) transplantation is widely used for treatment of blood disorders to re-establish long-term multi-lineage hematopoiesis. Enhance self-renewal potential of progenitor population to support hematopoiesis offer an alternative and complementary approach to achieve similar therapeutic effects. Nup98-Hoxa10hd fusion gene (NA) has been shown to confer expansion, anti-stress response and engraftment competitiveness on HSC. However, whether the ectopic expression of NA in multipotent progenitors (MPPs) could enhance their self-renewal potential and confer long-term multi-lineage hematopoiesis remains unknown. In this study, we showed that ectopic expression in MPPs confer long-term multi-lineage hematopoiesis in recipient mice. We further showed that NA upregulated pathways of cell cycle regulation, epigenetic regulation and response to stress in MPPs. These molecular traits increased the self-renewal potential of NA MPPs, which resulting in production of lineage-maintaining committed progenitor cells. Transcriptome analysis of NA myeloid progenitors identified genes regulating hematopoiesis, homeostasis, phosphorylation. In summary, we show that ectopic expression of Nup98-Hoxa10hd fusion gene enhance self-renwal potential of MPPs thus confer long-term multilineage repopulating capacity on MPPs, offering promising means to involve MPPs to augment cell source in clinical transplantation settings.

2020-10-06 | GSE146779 | GEO

Dynamic Gene Expression Response to TGF-b Stimulation in Multipotent Progenitors and Common Dendritic Cell Progenitors

Project description:Multipotent progenitors (MPP) and common dendritic cell progenitors (CDP) were obtained from mouse bone marrow, followed by in vitro culture with a specific cytokine cocktail and FACS sorting (Felker et al., 2010; Sere et al., 2012). Cells were treated with 10 ng/ml recombinant human TGF-b1 (R&D Systems, Minneapolis, USA) for 2, 4, 8, 12 and 24 h as described (Felker et al., 2010) or left untreated. Untreated multipotent progenitor (MPP) - MPP_0h_1 - MPP_0h_2 - MPP_0h_3 TGF-beta1 treated (2 hours) MPP - MPP_2h_1 - MPP_2h_2 - MPP_2h_3 TGF-beta1 treated (4 hours) MPP - MPP_4h_1 - MPP_4h_2 - MPP_4h_3 TGF-beta1 treated (8 hours) MPP - MPP_8h_1 - MPP_8h_2 - MPP_8h_3 TGF-beta1 treated (12 hours) MPP - MPP_12h_1 - MPP_12h_2 - MPP_12h_3 TGF-beta1 treated (24 hours) MPP - MPP_24h_1 - MPP_24h_2 - MPP_24h_3 Untreated common dendritic cell progenitor (CDP) - CDP_0h_1 - CDP_0h_2 - CDP_0h_3 TGF-beta1 treated (2 hours) CDP - CDP_2h_1 - CDP_2h_2 - CDP_2h_3 TGF-beta1 treated (4 hours) CDP - CDP_4h_1 - CDP_4h_2 - CDP_4h_3 TGF-beta1 treated (8 hours) CDP - CDP_8h_1 - CDP_8h_2 - CDP_8h_3 TGF-beta1 treated (12 hours) CDP - CDP_12h_1 - CDP_12h_2 - CDP_12h_3 TGF-beta1 treated (24 hours) CDP - CDP_24h_1 - CDP_24h_2 - CDP_24h_3

2014-04-15 | E-GEOD-46109 | biostudies-arrayexpress

CD71+ HSC/MPP

Project description:CD71+ HSC/MPP

| PRJNA789602 | ENA

Enforced Expression of NUP98-HOXA10hd Fusion Gene in Multipotent Progenitors Support Long-term Hematopoiesis in primary mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-10-06 | GSE146781 | GEO

Nuclear Condensation of NUP98-Fusion Proteins drives leukemogenic gene expression NUP98-fusion protein drive oncogenic gene expression via nuclear/biomolecular condensation

Project description:NUP98-fusion proteins cause leukemia via unknown molecular mechanisms. All NUP98-fusion proteins share an intrinsically disordered region (IDR) featuring >35 repeats of Phenylalanine-Glycine (FG) in the NUP98 N-terminus. Conversely, C-terminal NUP98-fusion partners often have critical functions in gene control. Given these structural features we hypothesized that mechanisms of oncogenic transformation by NUP98-fusion proteins are hard-wired in their protein interactomes. Affinity purification coupled to mass spectrometry and confocal imaging of five distinct NUP98-fusion proteins revealed that conserved interactors were enriched for proteins involved in biomolecular condensation and that they co-localized with NUP98-fusion proteins in nuclear puncta. We developed biotinylated isoxazole-mediated condensome mass spectrometry (biCon-MS) to show that NUP98-fusion proteins alter the global composition of biomolecular condensates. An artificial FG-repeat-containing fusion protein phenocopied the nuclear localization patterns of NUP98-fusion proteins and their capability to drive oncogenic gene expression programs. Thus, we propose that IDR-containing fusion proteins uniquely combine biomolecular condensation with transcriptional control to induce cancer.

2020-12-23 | PXD022518 | Pride

transcriptional profiling of NUP98-CDX1, NUP98-CDX4 and EGFP overexpressing primitive mouse bone marrow cells

Project description:The first genetic hits towards leukemia are thought often to confer to the mutant clone a slight proliferative/survial advantage. These pre-malignant clones can then be maintained under physiological cues in normal pool for long periods. We have searched for this type of first genetic hits and found that ectopic expression of novel nucleoporin 98 (NUP98)-homeodomain fusion proteins in primitive bone marrow cells can induce long-lasting hematopoietic stem cell (HSC) activity in these cells. More specifically, NUP98-CDX1/2 was able to sustain HSC activity with high frequencies despite massive in vitro expansions and in vivo residence. Continual expression of NUP98-CDX1/2 did not perturb lymphoid, myeloid or erythroid/platelet differentiation and NUP98-CDX1/2 was able to reprogram committed progenitors into cells with attributes of HSC. Switching off of NUP98-CDX1/2 expression did not lead to “return” to normal HSC but acute differentiation. Related NUP98-CDX4 induced leukemia with the shortest latency ever reported for HOX transcription factors. In this case switching off of NUP98-CDX4 expression cured the full-blown leukemia and again the cured cells showed only transient repopulating activity in vivo. These two types of pre-leukemic cells generated here will provide useful models for elucidating the self-renewal mechanisms of HSC as well as leukemic stem cells. Total RNA from NUP98-CDX lines was compared to EGFP overexpressing lines. The experiment was done in triplicate.

2012-12-01 | E-GEOD-37900 | biostudies-arrayexpress

Inhibition of mitochondrial transcription by the neurotoxin MPP+

Project description:The neurotoxin MPP+ triggers cell death of dopamine neurons and induces Parkinson’s disease symptoms in mice and men, but the immediate transcriptional response to this neurotoxin has not been studied. We therefore treated human SH-SY5Y cells with a low dose (0.1 mM) of MPP+ and measured the effect on nascent transcription by precision run-on sequencing (PRO-seq). We found that transcription of the mitochondrial genome was significantly reduced already after 30 min, whereas nuclear gene transcription was unaffected. Inhibition of respiratory complex I by MPP+ led to reduced ATP production, that may explain the diminished activity of mitochondrial RNA polymerase. Our results show that MPP+ has a direct effect on mitochondrial function and transcription, and that other gene expression or epigenetic changes induced by this neurotoxin are secondary effects that reflect a cellular adaptation program.

2023-06-01 | GSE214243 | GEO

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