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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE196580 | 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]

2022-11-09 | GSE165424 | GEO

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.

2022-11-09 | GSE196582 | 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

Type I interferon (IFN) response in USP18 knockout in THP-1 AML cells [ATAC-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 accessibility when combined with depletion of USP18, one of major negative regulators for IFN signaling.

2022-11-09 | GSE165426 | 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 [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

USP18 is an essential regulator of muscle cell differentiation and maturation

2022-03-23 | GSE198794 | GEO

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