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Links from GEO DataSets

Items: 19

1.

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

(Submitter supplied) 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:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: CSV
Series
Accession:
GSE196581
ID:
200196581
2.

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

(Submitter supplied) 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:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE196582
ID:
200196582
3.

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

(Submitter supplied) 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:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
6 Samples
Download data: TXT
Series
Accession:
GSE196580
ID:
200196580
4.

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

(Submitter supplied) 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.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: CSV
5.

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

(Submitter supplied) 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.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: CSV
6.

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

(Submitter supplied) 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.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
16 Samples
Download data: TXT
Series
Accession:
GSE165427
ID:
200165427
7.

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

(Submitter supplied) 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:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: TXT
Series
Accession:
GSE165426
ID:
200165426
8.

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

(Submitter supplied) 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:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE165425
ID:
200165425
9.

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

(Submitter supplied) 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:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: CSV
Series
Accession:
GSE165424
ID:
200165424
10.

Single-cell transcriptomic analysis of tumor-infiltrated immune cells from myeloid-specific Usp18 knockout mice

(Submitter supplied) Ubiquitin specific peptidase 18 (USP18) inhibits type I interferon response and mediates ISG15-deconjugation. Here, we examined the role of USP18 in myeloid-linage cells in tumor development. B16F10 melanoma grown in control or myeloid-specific Usp18 knockout mice were analyzed. Single-cell transcriptomic analysis revealed that the profile of tumor-infiltrated immune cells were altered with Usp18 deletion. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE173705
ID:
200173705
11.

Two ISREs functioning cooperatively regulate ISG expression in West Nile virus infected IFNAR-/- MEFs

(Submitter supplied) We previously identified a subset of interferon stimulated genes (ISGs), including Irf7, Irf1, Oas1a and Oas1b, upregulated by a West Nile virus (WNV) infection in wildtype mouse embryo fibroblasts (MEFs) after viral proteins had inhibited type 1 interferon (IFN)-mediated JAK-STAT signaling and also in WNV-infected STAT1-/-, STAT2-/-, IFNAR-/-, IRF3-/-, IRF7-/-, and IRF3/7-/- MEFs. In this study, ISG upregulation by WNV infection was inhibited in RIG-I/MDA5-/- but not in single knockout MEFs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
12 Samples
Download data: XLSX
Series
Accession:
GSE182446
ID:
200182446
12.

USP18 is an essential regulator of muscle cell differentiation and maturation

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: TSV
Series
Accession:
GSE198794
ID:
200198794
13.

Slfn2 Regulates Type I Interferon Responses by Modulating the NFĸB Pathway

(Submitter supplied) We demonstrate that Slfn2 interacts with protein phosphatase 6 regulatory subunit 1 (PPP6R1), leading to reduced type I IFN-induced activation of nuclear factor kappa B (NFĸB) signaling, resulting in reduced expression of ISGs.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
10 Samples
Download data: TXT
Series
Accession:
GSE109991
ID:
200109991
14.

mRNA microarray analysis of gene changes in Huh7 cells treated with IFN-λ4, IFN-λ1 and IFN-α

(Submitter supplied) The change of gene expression in Huh7 cells treated with IFN-λ4, IFN-λ1 and IFN-α was analyzed at 0h, 6h and 16h after different interferon treatments.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16951
7 Samples
Download data: GPR
Series
Accession:
GSE83085
ID:
200083085
15.

Hepatocytes treated with IFN-alpha or IFN-gamma and acute hepatitis C

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Third-party reanalysis
Platforms:
GPL570 GPL6244
18 Samples
Download data: CEL
Series
Accession:
GSE38598
ID:
200038598
16.

Gene expression profiling of 6 acute hepatitis C patients

(Submitter supplied) Approximately 50% of patients with chronic hepatitis C (CHC) have a sustained virologic response (SVR) to treatment with pegylated interferon (pegINF)-α and ribavirin. Non-response to treatment is associated with constitutively increased expression of IFN-stimulated genes (ISGs) in the liver. Treatment of patients with acute hepatitis C (AHC) is more effective, with SVR rates >90%. We investigated mechanisms of the different responses of patients with CHC and AHC to pegIFN-α therapy. more...
Organism:
Homo sapiens
Type:
Expression profiling by array; Third-party reanalysis
Platform:
GPL570
8 Samples
Download data: CEL, TXT
Series
Accession:
GSE38597
ID:
200038597
17.

Gene expression profiling of primary human hepatocytes treated with IFN-alpha or IFN-gamma

(Submitter supplied) Approximately 50% of patients with chronic hepatitis C (CHC) have a sustained virologic response (SVR) to treatment with pegylated interferon (pegINF)-α and ribavirin. Non-response to treatment is associated with constitutively increased expression of IFN-stimulated genes (ISGs) in the liver. Treatment of patients with acute hepatitis C (AHC) is more effective, with SVR rates >90%. We investigated mechanisms of the different responses of patients with CHC and AHC to pegIFN-α therapy. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
10 Samples
Download data: CEL
Series
Accession:
GSE38147
ID:
200038147
18.

The hypoxia-inducible transcription factor ZNF395 is controlled by I-kappaB kinase and activates genes involved in the innate immune response and cancer

(Submitter supplied) Activation of the hypoxia inducible transcription factor HIF-alpha and the NF-kappaB pathway promotes inflammation mediated tumor progression. The cellular transcription factor ZNF395 was repeatedly found over expressed in various human cancers and particularly in response to hypoxia, implying a functional relevance. To understand the biological activity of ZNF395, we identified target genes of ZNF395 by a genome-wide expression screen. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5381
Platform:
GPL6244
8 Samples
Download data: CEL
Series
Accession:
GSE44327
ID:
200044327
19.
Full record GDS5381

Transcription factor ZNF395 effect on RTS3b skin cancer cell line

Analysis of skin cancer cell line RTS3b-TR-ZNF395 following doxycycline-induced expression of FLAG-tagged ZNF395. Transcription factor ZNF395 is overexpressed in various human cancers, often in response to hypoxia. Results provide insight into the molecular effects of ZNF395 in skin cancer cells.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 protocol sets
Platform:
GPL6244
Series:
GSE44327
8 Samples
Download data: CEL
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