Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE37052 | GEO | 2012/09/19

SECONDARY ACCESSION(S): PRJNA157833

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

A FOXO3-IRF7 gene regulatory circuit limits inflammatory sequelae of antiviral responses.

Project description: Not available

| S-EPMC3556990 | biostudies-literature

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses

Project description:This SuperSeries is composed of the following subset Series: GSE36241: Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (ChIP-Seq) GSE37051: Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (expression) Refer to individual Series

2012-09-19 | E-GEOD-37052 | biostudies-arrayexpress

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (expression)

Project description:We have used an unbiased systems approach to predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. We detected significantly increased transcription of a subset of interferon-stimulated genes (ISGs) under basal conditions in Foxo3-null macrophages when compared to their wild type (WT) counterparts, suggesting that FOXO3 functions as a repressor of these genes. Stimulation of Foxo3-null macrophages with poly-IC (PIC) further increased the levels of this subset of ISGs, and also revealed the transcription of additional ISGs. C57BL/6 mice were obtained from Jackson Laboratories. Foxo3-/- mice in the FVB background were obtained from MMRRC and were backcrossed to C57BL/6 mice at least 5 times to generate congenic mice. C57BL/6 Foxo3+/- heterozygotes were intercrossed to generate Foxo3-/- mice. Mice were maintained at the animal facility of the Institute for Systems Biology and used at 8-12 weeks of age. All animals were housed and handled according to the approved protocols of the University of Washington and Institute for Systems Biology's Institutional Animal Care and Use Committees. Bone marrow macrophages from wildtype and Foxo3 knock-out mice were stimulated with PIC or left untreated. 3 replicates per group.

2012-09-19 | E-GEOD-37051 | biostudies-arrayexpress

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (ChIP-Seq)

Project description:We predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. Genome-wide location analysis combined with gene deletion studies identified the Irf7 gene as a critical target of FOXO3. FOXO3 was identified as a negative regulator of Irf7 transcription. Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechanism for establishing the requisite set points in the interferon pathway. C57BL/6 mice were obtained from Jackson Laboratories. Foxo3-/- mice in the FVB background were obtained from MMRRC and were backcrossed to C57BL/6 mice at least 5 times to generate congenic mice. C57BL/6 Foxo3+/- heterozygotes were intercrossed to generate Foxo3-/- mice. Mice were maintained at the animal facility of the Institute for Systems Biology and used at 8–12 weeks of age. All animals were housed and handled according to the approved protocols of University of Washington and Institute for Systems Biology's Institutional Animal Care and Use Committees.

2012-09-19 | E-GEOD-36241 | biostudies-arrayexpress

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (expression)

2012-09-19 | GSE37051 | GEO

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (ChIP-Seq)

2012-09-19 | GSE36241 | GEO

Swine IRF3/IRF7 attenuates inflammatory responses through TLR4 signaling pathway.

Project description: Not available

| S-EPMC5617478 | biostudies-literature

RNA-binding protein YTHDF3 suppresses interferon-dependent antiviral responses by promoting FOXO3 translation.

Project description: Not available

| S-EPMC6338863 | biostudies-other

Inflammatory monocytes hinder antiviral B cell responses.

Project description: Not available

| S-EPMC5111729 | biostudies-literature

A body-brain circuit regulating body inflammatory responses

Project description:The body-brain axis is emerging as a principal conductor of organismal physiology. It senses and controls organ function, metabolism and nutritional state. Here, we show that a peripheral immune insult powerfully activates the body-brain axis to regulate immune responses. We demonstrate that pro- and anti-inflammatory cytokines communicate with distinct populations of vagal neurons to inform the brain of an emerging inflammatory response. In turn, the brain tightly modulates the course of the peripheral immune response. Genetic silencing of this body-to-brain circuit produced unregulated and out-of-control inflammatory responses. By contrast, activating, rather than silencing, this circuit affords exceptional neural control of immune responses. We used single-cell RNA sequencing, combined with functional imaging, to identify the circuit components of this neuro-immune axis, and showed that its selective manipulation can effectively suppress the pro-inflammatory response while enhancing an anti-inflammatory state. The brain-evoked transformation of the course of an immune response offers new possibilities in the modulation of a wide range of immune disorders, from autoimmune diseases to cytokine storm and shock.

2024-04-11 | GSE263025 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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