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

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

PROVIDER: PRJNA611952 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11287638_1.fastq.gz	Fastqsanger.gz
	SRR11287638_2.fastq.gz	Fastqsanger.gz
	SRR11287639_1.fastq.gz	Fastqsanger.gz
	SRR11287639_2.fastq.gz	Fastqsanger.gz
	SRR11287640_1.fastq.gz	Fastqsanger.gz

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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

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 [MPP]

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

| PRJNA611951 | ENA

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:This SuperSeries is composed of the SubSeries listed below.

2020-10-06 | GSE146781 | GEO

Thermococcus barophilus MP strain:MP

Project description:Thermococcus barophilus MP strain:MP Genome sequencing and assembly

| PRJNA1234085 | ENA

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

MP-LRCC5314_gut_samples

Project description:MP-LRCC5314_gut_samples Metagenome

| PRJNA1055314 | ENA

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

NUP98-HOXA9 acute myeloid leukemia

Project description:Mass Spectrometry analysis of the interactome of the oncoprotein NUP98-HOXA9

2017-07-10 | PXD001828 | Pride