Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer

ABSTRACT: The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer

PROVIDER: PRJNA1158868 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30610723.fastq.gz	Fastqsanger.gz
	SRR30610724.fastq.gz	Fastqsanger.gz
	SRR30610725.fastq.gz	Fastqsanger.gz
	SRR30610726.fastq.gz	Fastqsanger.gz
	SRR30610727.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer [snRNA-Seq]

Project description:The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer [snRNA-Seq]

| PRJNA1215436 | ENA

The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer

Project description:Gene expression profile of STAT-signaling tumor-initiating cells (TIC) in breast xenograft models

2024-12-09 | GSE276789 | GEO

The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer [snRNA-Seq]

Project description:Gene expression profile of STAT-signaling tumor-initiating cells (TIC) in breast xenograft models

2025-01-24 | GSE288006 | GEO

Interferon-stimulated gene expression in STAT1 knockout cells

Project description:STAT1 plays a cental role in the induction of interferon-stimulated genes, but interferon alpha can activate a STAT1-independent pathway that leads to gene expression. We performed microarray analysis to examine whether like interferon alpha, interferon lambda, a newly discovered interferon, can induce the expression of interferon-stimulated genes in the absence of STAT1. Control and STAT1 knockout Huh-7.5 hepatoma cells were left untreated or treated with 1000 U/ml of human interferon alpha 2a or interferon lambda 1 (PBL) for 24 h, and total RNA was extracted. Sense-strand DNA was generated from 200 ng of total RNA, fragmented, and labeled using a GeneChip WT Plus Reagent Kit (Affymetrix). Six samples were obtained and each sample was anlyzed using one GeneChip.

2016-07-22 | E-GEOD-84693 | biostudies-arrayexpress

Modified Stat1 Confers Enhanced Interferon Responsiveness and Improved Baseline Antiviral Host Defense

Project description:U3A cells stably expressing wild-type STAT1 or STAT1-CC were treated with interferon beta (10U/ml) or control for 24 hours to assess effects of stat1 modifications, interferon, and the interaction on gene expression. Keywords: interferon, STAT1, STAT1-CC, STAT1CC, STAT-1C, antiviral RNA was isolated from stable U3A-STAT1 lines stably expressing wild-type STAT1 or STAT1CC, after 24 hour treatment with interferon beta (10U/ml) or control.

2015-09-01 | E-GEOD-61413 | biostudies-arrayexpress

Interferon-stimulated gene expression in STAT1 knockout cells

2016-07-22 | GSE84693 | GEO

hCAF1/CNOT7 regulates interferon signaling by targeting STAT1

Project description:Stringent regulation of the interferon signaling pathway is essential for maintaining the immune response to pathogens and tumors. The transcription factor STAT1 is a crucial mediator of this response. Here we show that hCAF1/CNOT7 regulates class I and II interferon pathways at different crucial steps. In resting cells hCAF1 can control STAT1 trafficking by interacting with the latent form of STAT1 in the cytoplasm. IFN treatment induces STAT1 release, suggesting that hCAF1 may shield cytoplasmic STAT1 from undesirable stimulation. Consistent, hCAF1 silencing enhances STAT1 basal promoter occupancy associated with increased expression of a subset of STAT1-regulated genes. Consequently, hCAF1 knockdown cells exhibit an increased protection against viral infection and reduced viral replication. Furthermore, hCAF1 participates in the extinction of the IFN signal, through its deadenylase activity, by speeding up the degradation of some STAT1-regulated mRNAs. Since abnormal and unbalanced JAK/STAT activation is associated with immune disorders and cancer, hCAF1 could play a major role in innate immunity and oncogenesis, contributing to tumor escape. mRNAs from cells expressing the siRNA siRNA duplexes targeting hCAF1, corresponding to the coding region 941-961 (kd) (hCAF1 NCBI Reference Sequence: NM_013354.5) and one non-targeting control siRNA (mock).

2013-12-31 | E-GEOD-43334 | biostudies-arrayexpress

Modified Stat1 Confers Enhanced Interferon Responsiveness and Improved Baseline Antiviral Host Defense

2015-09-01 | GSE61413 | GEO

hCAF1/CNOT7 regulates interferon signaling by targeting STAT1

2013-12-31 | GSE43334 | GEO

Interferon signature in patients with STAT1 gain-of-function mutation is epigenetically determined

Project description:STAT1 gain-of-function (GOF) variants lead to defective Th17 cell development and chronic mucocutaneous candidiasis (CMC), but frequently also to autoimmunity. STAT1 GOF mutations result in hyperphosphorylation and delayed dephosphorylation of STAT1. However, how the delayed dephosphorylation exactly causes the increased expression of STAT1-dependent genes, and how the intracellular signal transduction from cytokine receptors is affected, remains unknown. In this study we show that the circulating levels of IFN-α in STAT1 GOF patients were not persistently elevated. Nevertheless, the interferon signature was evident even in the patient with low or undetectable IFN-α levels. Chromatin immunoprecipitation (ChIP) experiments showed that the active chromatin mark H3K4me3, was significantly enriched in areas associated with interferon-stimulated genes in STAT1 GOF cells in comparison to normal cells. This suggests that GOF STAT1, while binding to chromatin, promotes epigenetic changes compatible with higher gene expression and elevated reactivity to type I interferons, and interferon-related autoimmunity. We suggest that epigenetic rewiring may be responsible for treatment failure of JAK1/2 inhibitors in certain patients. We also found that after IL-21 stimulation the balance of p-STAT3/p-STAT1 was significantly impaired in patients, which could potentially be applied as a diagnostic test for STAT1 GOF.

2019-05-31 | GSE120580 | GEO

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