Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of liver from mice deficient for IFNg or both IFNg and Suppressor of Cytokine Signalling-1 at 0.5 to 48 hours after INFg treatment

ABSTRACT: Timecourse analysis of Interferon-Gamma (IFNg) signalling in mice deficient for IFNg or both IFNg and Suppressor of Cytokine Signalling-1 (SOCS1).

ORGANISM(S): Mus musculus

SUBMITTER: Sam Wormald

PROVIDER: E-GEOD-4232 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

The comparative roles of suppressor of cytokine signaling-1 and -3 in the inhibition and desensitization of cytokine signaling.

Wormald Samuel S Zhang Jian-Guo JG Krebs Danielle L DL Mielke Lisa A LA Silver Jeremy J Alexander Warren S WS Speed Terence P TP Nicola Nicos A NA Hilton Douglas J DJ

The Journal of biological chemistry 20060210 16

Negative feedback is a mechanism commonly employed in biological processes as a means of maintaining homeostasis. We have investigated the roles of suppressor of cytokine signaling (SOCS) proteins in regulating the kinetics of negative feedback in response to cytokine signaling. In mouse livers and bone marrow-derived macrophages, both interferon-gamma (IFNgamma) and interleukin-6 (IL-6) rapidly induced the tyrosine phosphorylation of signal transducer and activator of transcription-1 (STAT1) an ...[more]

PMID: 16473883

Similar Datasets

Interferon-gamma timecourse in IFNg-/- and SOCS1-/-IFNg-/- mouse livers

Project description:Timecourse analysis of Interferon-Gamma (IFNg) signalling in mice deficient for IFNg or both IFNg and Suppressor of Cytokine Signalling-1 (SOCS1). Keywords: time course expression analysis

2006-02-14 | GSE4232 | GEO

IFNg+ vs IFNg- Treg

Project description:Gene expression studies comparing IFNg+ Tregs versus IFNg- Tregs from human peripheral blood Ex vivo sorted Tregs (CD25highCD127neg) were stimulated for 4 hours and IFNg-secreting cells were detected by a IFNg-capture kit. The samples were resorted based on IFNg expression.

2016-07-01 | E-GEOD-71274 | biostudies-arrayexpress

The tumor suppressor SOCS1 diminishes tolerance to oxidative stress in hepatocellular carcinoma

Project description:SOCS1 is a tumor suppressor in hepatocellular carcinoma. Recently we showed that loss of SOCS1 in hepatocytes promotes NRF2 activation. Here we investigated how SOCS1 expression affected oxidative stress response in HCC cells. Murine Hepa1-6 cells expressing SOCS1 (Hepa-SOCS1) or control vector (Hepa-Vector) were treated with cisplatin or tert-butyl hydroperoxide (t-BHP). Induction of NRF2 and its target genes, oxidative stress, lipid peroxidation, cell survival and cellular proteome profiles were evaluated. NRF2 induction was significantly reduced in Hepa-SOCS1 cells. The gene and protein expression of NRF2 targets were differentially induced in Hepa-Vector cells but markedly suppressed in Hepa-SOCS1 cells. Hepa-SOCS1 cells displayed increased induction of reactive oxygen species (ROS) but reduced lipid peroxidation. Nonetheless, Hepa-SOCS1 cells treated with cisplatin or t-BHP showed reduced survival. GCLC, poorly induced in Hepa-SOCS1 cells, showed a strong positive correlation with NFE2L2 and an inverse correlation with SOCS1 in the TCGA-LIHC transcriptomic data. Proteomic analysis of Hepa-Vector and Hepa-SOCS1 cells revealed that SOCS1 differentially modulated many proteins involved in diverse molecular pathways including those implicated in mitochondrial ROS generation and detoxification by peroxiredoxin and thioredoxin systems. Our findings indicate that maintaining sensitivity to oxidative stress is an important tumor suppression mechanism of SOCS1 in HCC.

2024-05-22 | PXD047908 | Pride

IFNg+ vs IFNg- Treg

Project description:Gene expression studies comparing IFNg+ Tregs versus IFNg- Tregs from human peripheral blood

2016-07-01 | GSE71274 | GEO

IFNg-/- and conditional Socs3-/- mice: cytokine treatments

Project description:Changes in mouse liver mRNA profiles following intraperitoneal cytokine injection. Either interferon-gamma-/-, albumin-cre(-) Socs3(w/fl) mice, or albumin-cre(+) Socs3(-/fl) mice were injected with either phosphate-buffered saline, interferon-gamma, or interfeukin-6, and livers taken after 4h. Keywords = Socs3, interferon gamma, interleukin-6, il6, liver, suppressor of cytokine signalling 3 Keywords: repeat sample

2003-04-10 | GSE369 | GEO

Transcription profiling of mouse wild type and Pias1 null cells in response to IFN treatments to study the effect of PIAS1 on interferon (IFN) signaling pathway

Project description:Microarray analysis was designed to study the effect of PIAS1 on interferon (IFN) signaling pathway by comparing the gene activation profiles of wild type and Pias1 null cells in response to IFN treatments. Microarray analysis was performed essentially following the manufacturer's instructions (Affymetrix). Briefly, bone marrow-derived macrophages (BMMs) from wile type or Pias1 null littermates were either untreated, or treated with IFN-beta (500 U/ml) or IFN-gamma (10 ng/ml) for 2h or 4h. Total RNA was prepared with RNA-STAT60 (TEL-TEST) and purified with the RNeasy kit (Qiagen). Double stranded complementary DNA was synthesized from 20 ug of total RNA according to Affymetrix methodology, and purified with Phase Lock Gels (Eppendorf). Biotin-labeled RNA was synthesized with the BioArray High Yield RNA Transcript Labeling Kit (Enzo). Samples were cleaned, fragmentated and hybridized to murine genome (MGU74Av2) Genechips (Affymetrix) as instructed. GeneChips were stained with phycoerythrin-streptavidin (Molecular Probes) and scanned with a GeneChip scanner (Affymetrix).

2007-10-10 | E-GEOD-1552 | biostudies-arrayexpress

IFNg treatment of monocytes

Project description:IFNg treatment of monocytes

| PRJNA597901 | ENA

Mus musculus

Project description:Interferon-gamma timecourse in IFNg-/- and SOCS1-/-IFNg-/- mouse livers

| PRJNA94885 | ENA

Human IFNG+/- Treg and Tconv transcriptome

Project description:Microarray used to detail the global gene transcription underlying sorted IFNg+ and IFNg- Tregs (CD4+CD25+CD127lo) and Tconv (CD4+CD25-CD127+) for fresh (unexpanded) and 14 day expanded cells from human blood. Treg and Tconv were FACS isolated from five healthy subjects (median age of 26, range 22-30). Sorted cells were separated into two groups: the first group was stimulated for 4 hours with PMA/ionomycin and labeled with the IFNg cytokine capture kit (Miltenyi Biotech) followed by FACS isolation of IFNg- and IFNg+ populations. The second set was expanded to day 14 prior to reactivation and cytokine cell capture. For each IFNg sorted population, cells were pelleted and flash frozen before RNA isolation and processing.

2015-05-01 | E-GEOD-59786 | biostudies-arrayexpress

IFNg shapes macrophage inflammatory responses by STAT1 isoform-specific epigenetic and transcriptional mechanisms

Project description:Interferon gamma (IFNg) is a pivotal cytokine that activates macrophages and shapes their response to subsequent inflammatory stimuli. Here, we investigated the distinct roles of STAT1 isoforms, STAT1alpha and STAT1beta, in IFNg-induced epigenetic remodelling and subsequent responses to lipopolysaccharide (LPS) in primary macrophages. We show that the STAT1 C-terminal TAD, which is missing in the STAT1beta isoform, is required for both H3K27 acetylation and deacetylation in response to IFNg. Notably, H3K27 deacetylation was associated with AP-1 motifs rather than STAT1 binding, suggesting indirect regulatory mechanisms. Functionally, IFNg pretreatment suppressed the induction of anti-inflammatory and virus response genes, including a subset of IFN-stimulated genes (ISGs), in response to LPS, while enhancing the expression of a distinct set of ISGs. Mechanistically, the STAT1 C-terminal TAD was critical for IFNg-mediated inhibition of LPS-induced enhancer activation at key regulatory genes, such as Il10 and Irak3, which are involved in negative feedback of toll-like receptor (TLR) signalling. Conversely, cooperative gene activation by IFNg and LPS was largely independent of the STAT1 C-terminal TAD, with notable exceptions, such as Ido1 and Tgtp1. Genome-wide analysis indicated that IRF1 and IRF8, rather than STAT1 homodimers, predominantly mediate in IFNg-induced H3K27 acetylation and transcription factor network analysis identified additional regulators integrating IFNg and LPS responses. Together, these findings reveal gene- and isoform-specific roles of STAT1 in coordinating IFNg-dependent chromatin remodelling and transcriptional cross-regulation, providing new insights into the control of inflammation and innate immunity.

2025-09-30 | GSE309503 | 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