Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The transcriptomic analysis for Usp18 homozygous depletion in established AML1/ETO 9a leukemia mouse model [AE9a_scRNA-seq II]

ABSTRACT: Usp18 is a potent negative reguator of type I IFN signaling. However, it is not well characterized how Usp18 affects IFN stimulated genes (ISGs) induction in AML in mouse model. Here, we analyzed the transcriptomic data when combined with homozygous depletion of USP18, which phenotypicaly reduce AE9a leukemia progression.

ORGANISM(S): Mus musculus

PROVIDER: GSE196582 | GEO | 2022/11/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The transcriptomic analysis for Usp18 heterozygous depletion in established AML1/ETO 9a leukemia mouse model [AE9a_scRNA-seq]

Project description:Usp18 is a potent negative reguator of type I IFN signaling. However, it is not well characterized how Usp18 affects IFN stimulated genes (ISGs) induction in AML in mouse model. Here, we analyzed the transcriptomic data when combined with heterozygous depletion of USP18, which phenotypicaly reduce AE9a leukemia progression.

2022-11-09 | GSE165425 | GEO

The transcriptomic analysis for Usp18 heterozygous depletion in established AML1/ETO 9a leukemia mouse model [AE9a_RNA-seq]

2022-11-09 | GSE165424 | GEO

The transcriptomic analysis for Usp18 heterozygous depletion in established AML1/ETO 9a leukemia mouse model [AE9a_RNA-seq II]

2022-11-09 | GSE196581 | GEO

The ATAC analysis for Usp18 heterozygous depletion in established AML1/ETO 9a leukemia mouse model

Project description:Type I IFN induces IFN stimulated genes (ISGs) and exert varieties of immunomoduratory functions. However, it is not well characterized how ISGs are regulated by negative regulators of IFN signaling. Here, we analyzed the chromatin accessibility when combined with depletion of USP18, one of major negative regulators for IFN signaling.

2022-11-09 | GSE196580 | GEO

Type I interferon (IFN) response in USP18 knockout in THP-1 AML cells [RNA-seq]

Project description:Type I IFN induces IFN stimulated genes (ISGs) and exert varieties of immunomoduratory functions. However, it is not well characterized how ISGs are regulated by negative regulators of IFN signaling. Here, we analyzed the transcriptomic data when combined with depletion of USP18, one of major negative regulators for IFN signaling.

2022-11-09 | GSE165428 | GEO

Type I interferon (IFN) response in USP18 knockout in THP-1 AML cells [ATAC-seq]

2022-11-09 | GSE165426 | GEO

Rosa26-AML1-ETO 9a knock-in pre-leukemic Lin-cKit+ (LK) single-cell RNA sequencing

Project description:T(8;21), which produces the AML1-ETO (AE) fusion oncoprotein, is one of the most common chromosomal abnormalities in AML patients. Despite its prevalence among patients, it has remained challenging to study the impact of AE on leukemia development in vivo due to limitations of the current t(8;21) mouse models. Here, we devised a germline transmitted transgenic Rosa26-AE9a knock-in mouse model that expresses AE9a protein, a truncated AE variant, at moderately elevated levels compared to endogenous RUNX1. These mice develop myeloid leukemia with longer latency and lower penetrance compared to mice using the AE9a retroviral transduction-transplantation model. Pre-leukemic mice exhibited myeloid progenitor skewing in their bone marrow, with more granulocyte-monocyte progenitors (GMP) at the expense of megakaryocyte-erythroid progenitors (MEP). Importantly, hematopoietic stem and progenitor cells (HSPCs) of pre-leukemic mice had increased clonogenic potential. We performed single cell RNA-sequencing on pre-leukemic HSPCs and confirmed both this granulocytic bias and hindered differentiation. Overall, we have overcome the limitation of uncontrolled AE9a oncogene expression in the retroviral transduction-transplantation mouse model and have devised a new germline transmitted Rosa26 locus AE9a knock-in model that more faithfully represents t(8;21) human disease.

2023-10-11 | GSE173712 | GEO

Type I interferon (IFN) response in USP18 knockout in THP-1 AML cells [ChIP-seq]

Project description:Type I IFN induces IFN stimulated genes (ISGs) and exert varieties of immunomoduratory functions. However, it is not well characterized how ISGs are regulated by negative regulators of IFN signaling. Here, we analyzed the chromatin activity using H3K27Ac ChIP when combined with depletion of USP18, one of major negative regulators for IFN signaling.

2022-11-09 | GSE165427 | GEO

Type I interferon (IFN) response in USP18 knockout in MDA-MB-231 breast cancer cells [RNA-seq]

Project description:Type I IFN induces IFN stimulated genes (ISGs) and exert varieties of immunomoduratory functions. However, it is not well characterized how ISGs are regulated by negative regulators of IFN signaling. Here, we analyzed the transcriptomic change when combined with depletion of USP18, one of major negative regulators for IFN signaling.

2022-11-09 | GSE165429 | GEO

USP18-dependent muscle proteome

Project description:USP18 is an interferon type 1 (IFN-1) induced gene that negatively regulates the IFN-1 signalling pathway, which plays a role in many immune related pathologies. Dermatomyositis (DM) is characterised by excessive IFN-1 immune response and muscle degeneration. We found USP18 to be expressed in DM myofibers suggesting a role in muscle cell biology. USP18 depletion induced muscle cell differentiation under nutrient-rich conditions independent of IFN-1 signalling. Downregulation of cell cycle gene network and sarcomeric protein networks, and dysregulation of myogenic (co-)transcription regulators were found in USP18-depleted differentiated cells. Sarcomeric integrity of USP18-depleted cells deteriorated during muscle cell maturation. Our results revealed USP18 as a critical regulator at the intersection between proliferation and differentiation as well as during the maturation of muscle cells. We suggest that a USP18 IFN-1-independent pathway may contribute to muscle regeneration in muscle pathologies.

2023-05-10 | PXD032406 | Pride

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