Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeting nucleoporin 214 selectively eliminates leukemia stem cells

ABSTRACT: LSCs from MLL-AF9-driven Nup214fl/fl and Nup214fl/fl,Tie2-Cre AML mice were sorted, followed by further proteomic assay.

INSTRUMENT(S): Bruker Daltonics timsTOF series

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Bone Marrow

SUBMITTER: Zhe Chen

LAB HEAD: Zhe Chen

PROVIDER: PXD054471 | Pride | 2025-07-26

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	FE235SC_HET_1.zip	Other
	FE235SC_HET_3.zip	Other
	FE235SC_HET_4.zip	Other
	FE235SC_HET_5.zip	Other
	FE235SC_WT_2.zip	Other

Items per page:

1 - 5 of 10

Similar Datasets

Targeting KPNB1 suppresses DNA damage repair in AML cells by inhibiting HMGB2 nuclear translocation

Project description:To gain insight into the potential cargo proteins mediated by KPNB1, the nuclear fraction of DMSO- and IPZ-treated NB-4 cells were isolated and then subjected to mass spectrometry analysis.

2025-01-03 | PXD056172 | Pride

Targeting nucleoporin 214 selectively eliminates leukemia stem cells

Project description:To profile the E3 ligase associated with NUP214 neddylation, the NUP214 co-IP sample in THP-1 cells were examined by mass spectrometry.

2025-07-26 | PXD054462 | Pride

Targeting nucleoporin 214 selectively eliminates leukemia stem cells

Project description:To illustrate NUP214-interacting proteins, we performed co-immunoprecipitation (co-IP) followed by mass spectrometry using MLL-AF9-driven LSCs to characterize protein interactomes of NUP214.

2025-07-26 | PXD054438 | Pride

Role of Pfn-1 phosphorylation in gene expression in glioma-associated endothelial cells

Project description:Analysis of gene expression in glioma-associated endothelial cells in Tie2-Cre,Pfn1fl/fl:Y129F and Pfn1fl/fl:Y129F mice We detected different gene expression patterns in the tumor-associated endothelial cells in Tie2-Cre,Pfn1fl/fl:Y129F and Pfn1fl/fl:Y129F mice

2014-02-25 | GSE55295 | GEO

Role of Pfn-1 phosphorylation in gene expression in glioma-associated endothelial cells

2014-02-25 | E-GEOD-55295 | biostudies-arrayexpress

Endothelial RNF20 regulates the self-renewal and differentiation of neural precursor cells during embryonic development

Project description:Purpose: To further explore how endothelial RNF20 regulates embryonic neurogenesis, RNA isolated from the endothelial cells of RNF20fl/fl and RNF20cKO-Tie2 brain cortex at E13 was analyzed by RNA-seq to determine the genome-wide changes. Methods: mRNA from E13 isolated endothelial cells of RNF20fl/fl and RNF20cKO-Tie2 mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, mRNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Approximately one thousand transcripts showed differential expression between the RNF20fl/fl and RNF20cKO-Tie2 mice brain cortex, with a fold change ≥2 and p value <0.05. Gene ontology analysis of downregulated genes showed the genes were enriched in terms related to neuron differentiation, cell communication and secretion by cells.Concomitantly, upregulated genes were enriched in terms related to negative regulation of cytokine production and cell development.The results showed that endothelial RNF20 is critical for neurogenesis. Conclusions: Endothelial RNF20 RNA-seq would provide a overall understanding how endothelial RNF20 regulates the self-renewal and differentiation of neural precursor cells during embryonic development

2022-01-07 | GSE192997 | GEO

FoxM1 is essential for quiescence and maintenance of hematopoietic stem cell

Project description:FoxM1, a mammalian Forkhead Box M1 protein, is known as a typical proliferation-associated transcription factor that regulates of G1/S and G2/M transition in the proliferating cells. However, the in vivo function of FoxM1 in adult stem cells remains unknown. Here, we found that FoxM1 is highly expressed in hematopoietic stem cells (HSCs) and is essential for maintaining quiescence and self-renewal of HSCs in vivo. FoxM1-deficient mice developed leukopenia, thrombocytopenia and neutropenia with an approximately 6-fold decrease in HSC pool size, which is associated with a failure of G0 cell cycle regulation and increased cell cycling in HSCs. FoxM1 absence did not affect lineage commitment of HSCs and progenitors. However, FoxM1 loss significantly reduced the repopulating capacity and self-renewal of long-term HSC in a cell-autonomous manner. Mechanistically, FoxM1 loss markedly down-regulates the expression of orphan nuclear receptor Nurr1, known to regulate HSC quiescence. We found that FoxM1 directly bound the promoter region of Nurr1 and induced transcriptional activity of Nurr1 promoter in vitro, and forced expression of Nurr1 rescued FoxM1-deletion-induced G0 loss of HSC-enriched population in vitro. Thus, our studies show a previously unrecognized role of FoxM1 as a critical regulator of HSC quiescence and self-renewal by controlling Nurr1-mediated pathways. The Hematopoietic Stem Cells (HSCs) were sorted from FoxM1[fl/fl] and Tie2-Cre FoxM1[fl/fl] mice, then amplified with Ovation Pico WTA System V2 before microarray analysis. There are 3 samples from FoxM1[fl/fl]mice and 3 samples from Tie2-Cre FoxM1[fl/fl] mice.

2015-06-15 | E-GEOD-62360 | biostudies-arrayexpress

Microbiota-driven arginase 1 expression impedes the resolution of intestinal inflammation

Project description:Arginase 1 (Arg1), which converts L-arginine into ornithine and urea, exerts pleiotropic immunoregulatory effects. Patients with inflammatory bowel disease (IBD) show an enhanced expression and activity of Arg1 in the intestinal (sub-)mucosa, but the function of Arg1 in IBD remains poorly characterized. Here, we found that Arg1 expression correlates with the degree of inflammation in colitic tissues of IBD patients. In mice with - experimental colitis Arg1 was upregulated in an IL-4-/IL-13- and intestinal microbiota-dependent manner. Tie2-Cre+/-Arg1fl/fl mice lacking Arg1 in hematopoietic and endothelial cells recovered faster from colitis than Arg1-expressing littermates. This correlated with decreased vessel density, compositional changes in the intestinal microbiota, diminished infiltration by myeloid cellsand an accumulation of intraluminal polyamines that are associated with epithelial healing. Dietary L-arginine restriction abolished the protective effect of Arg1-deletion, suggesting that protection is related to an increased availability of L-arginine. Fecal microbiota transfers from Tie2-Cre+/-Arg1fl/fl mice into wildtype recipients restored the protective, anti-inflammatory phenotype while transfers from wildtype littermates into Arg1-deficient mice prevented the accelerated recovery from colitis. Thus, altered intestinal microbiota and metabolic products in Tie2-Cre+/-Arg1fl/fl mice account for the accelerated resolution from colitis in the absence of Arg1. Subsequently, L-arginine serves as novel therapeutic and diagnostic target for clinical intervention in IBD patients.

2020-06-07 | GSE151931 | GEO

EMP1 preserves hematopoietic stem cell potential under homeostasis and radiation-induced injury by alleviating ER stress

Project description:To illustrate EMP1-interacting proteins, we performed co-immunoprecipitation (co-IP) followed by mass spectrometry using HSPCs (Lin-c-Kit+) to characterize protein interactomes of EMP1. Murine HSPCs (Lin-c-Kit+) were infected with retrovirus to force EMP1 overexpression (with HA tag). Then IgG or HA antibodies were used to conducted co-immunoprecipitation (co-IP), followed by and mass spectrometry analysis.

2025-03-13 | PXD055884 | Pride

Proteomic analysis of Streptococcus mutans after RpoA-K173R mutation

Project description:Functional experiments have found a significant increase in EPS synthesis upon the elimination of lactylation at RpoA Lys173. Thus we investigated the regulatory mechanisms by proteomic approah.

2023-08-24 | PXD042680 | Pride