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

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 heterozygous depletion of USP18, which phenotypicaly reduce AE9a leukemia progression.

ORGANISM(S): Mus musculus

PROVIDER: GSE165424 | GEO | 2022/11/09

REPOSITORIES: GEO

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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 II]

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

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 homozygous depletion of USP18, which phenotypicaly reduce AE9a leukemia progression.

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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.

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

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

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

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

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

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

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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]

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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.

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