Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of a novel role for FoxO3 isoform2 in osteoclastic inhibition

ABSTRACT: Identification of a novel role for FoxO3 isoform2 in osteoclastic inhibition

PROVIDER: PRJNA559068 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9915513.fastq.gz	Fastqsanger.gz
	SRR9915514.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Identification of a novel role for FoxO3 isoform2 in osteoclastic inhibition

Project description:We performed RNA-seq experiments, one with the WT control and Foxo3KO osteoclast precursors after RANKL stimulation to identify genes regulated by Foxo3 in osteoclast precursors.

2019-09-25 | GSE135479 | GEO

Identification of a Novel Role for Foxo3 Isoform2 in Osteoclastic Inhibition.

Project description: Not available

| S-EPMC6783374 | biostudies-literature

Expression data of the human multiple myeloma cell line MM1.S after AKT inhibition in a FOXO3 deficient background

Project description:Forkhead box O transcription factors are important downstream targets of AKT signalling. In the human Multiple Myeloma celline MM1.S, AKT inhibtion leads to cell death in a FOXO3 dependent fashion. We used microarrays to asses which genes are up- or downregulated by FOXO3 after AKT inhibition by MK2206.

2020-09-02 | GSE120939 | GEO

Expression data of the human multiple myeloma cell line XG-3 after AKT inhibition in a FOXO3 deficient background

Project description:Forkhead box O transcription factors are important downstream targets of AKT signalling. In the human Multiple Myeloma celline XG-3, AKT inhibtion leads to cell death in a FOXO3 dependent fashion. We used microarrays to asses which genes are up- or downregulated by FOXO3 after AKT inhibition by MK2206.

2020-09-02 | GSE120938 | GEO

Role of FoxO3 in adult neural stem cell maintenance in mice

Project description:In the nervous system, neural stem cells (NSC) are necessary for the generation of new neurons and for cognitive function. Here we show that FoxO3, a member of a transcription factor family known to extend lifespan in invertebrates, regulates the NSC pool. We find that adult FoxO3-/- mice have fewer NSC in vivo than wild type counterparts. NSC isolated from adult FoxO3-/- mice have decreased self-renewal and an impaired ability to generate different neural lineages. Identification of the FoxO3-dependent gene expression profile in NSC suggests that FoxO3 regulates the NSC pool by inducing a program of genes that preserves quiescence, prevents premature differentiation, and controls oxygen metabolism. The ability of FoxO3 to prevent the premature depletion of NSC might have important implications for counteracting brain aging in long-lived species.

2009-11-29 | GSE18326 | GEO

Foxo3 drives pathogenic Th1 differentiation

Project description:We showed that the transcription factor Foxo3 played a specific role in the polarization of CD4+ T cells towards pathogenic Th1 cells producing both interferon-γ (IFN-γ) and granulocyte monocyte colony stimulating factor (GM-CSF). To understand the molecular mechanisms whereby Foxo3 controls CD4+ T cell differentiation, unbiased analysis of genes differentially expressed in Foxo3-deficient vs. Foxo3-sufficient CD4+ T cells was achieved using both resting and activated CD4+ T cells obtained following 12 or 24 hours of stimulation with anti-CD3 mAbs.

2016-09-01 | GSE86287 | GEO

FOXO1 and FOXO3

Project description:FOXO1 and FOXO3

| PRJNA495066 | ENA

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.

2012-09-19 | GSE36241 | GEO

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 (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

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