E-MTAB-5445
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-5445 | ExpressionAtlas | 2017-02-09
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-5445-analysis-methods.tsv | Tabular | |||
| E-MTAB-5445-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-5445-configuration.xml | Xml | |||
| E-MTAB-5445-percentile-ranks.tsv | Tabular | |||
| E-MTAB-5445.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 56 |
Similar Datasets
Project description:We report transcript abundance in murine bone marrow-derived macrophages (BMDMs) upon Rickettsia parkeri infection and treatment with type I interferon (IFN-I). Infections and IFN-I treatment were performed in parallel between WT BMDMs and BMDMs lacking genes encoding interferon-responsive factor (IRF) transcription factors, including IRF1, IRF5, and double mutant cells lacking both IRF3 and IRF7. Control cells were uninfected and not treated with IFN-I. The abundance of transcripts between these cells can be compared in order to identify genes specifically regulated by each IRF upon IFN-I treatment.
2019-07-04 | GSE128211 | GEO
Project description:Interferon regulatory factor 5 expression levels regulate murine lupus in a type-I interferon-independent manner
| PRJNA119861 | ENA
Project description:The transcription factor NF-κB has been associated with a range of pathological conditions of the heart, mainly based on its function as a master regulator of inflammation and pro-survival factor. Here, we addressed the question what effects activation of NF-κB can have during murine heart development. We expressed a constitutively active (CA) mutant of IKK2, the kinase activating canonical NF-κB signaling, specifically in cardiomyocytes under the control of the α-myosin heavy chain promoter. Expression of IKK2-CA resulted in embryonic lethality around E13. Embryos showed defects in compact zone formation and the contractile apparatus, and overall were characterized by widespread inflammation with infiltration of myeloid cells. Gene expression analysis at E12.5 suggested an interferon type I signature, with increased expression of interferon regulatory factors.
2015-10-14 | E-MTAB-3971 | biostudies-arrayexpress
Project description:We report the response of murine hepatic macrophages to chronic CCl4 administration in wild-type mice and mice with a myeloid-specific deletion of interferon regulatory factor 5
2017-08-24 | GSE82157 | GEO
Project description:Regulatory Role of SLFN5 in Type I Interferon Signaling
| PRJNA348531 | ENA
Project description:Distinct immune responses to type I and III interferons are regulated by interferon regulatory factor 1
| PRJNA474093 | ENA
Project description:Polymorphisms in the transcription factor interferon regulatory factor 5 (IRF5) are strongly associated in human genetic studies with an increased risk of developing the autoimmune disease systemic lupus erythematosus. However, the biological role of IRF5 in lupus pathogenesis, if any, is not known. In this study we show that IRF5 is absolutely required for disease development in the FcgRIIB-/-Yaa and FcgRIIB-/- lupus models. In contrast to IRF5-sufficient FcgRIIB-/-Yaa mice, IRF5-deficient FcgRIIB-/-Yaa mice do not develop lupus manifestations and have a phenotype comparable to wildtype mice. Strikingly, full expression of IRF5 is required for the development of autoimmunity, as IRF5-heterozygotes had dramatically reduced disease. One effect of IRF5 is to induce the production of the type I interferon IFN-gamma, a cytokine implicated in lupus pathogenesis. To address the mechanism by which IRF5 promotes disease, we evaluated FcgRIIB-/-Yaa mice lacking the type I interferon receptor IFNAR1. Unlike the IRF5-deficient and IRF5-heterozygous FcgRIIB-/-Yaa mice, IFNAR1-deficient FcgRIIB-/-Yaa mice maintained a substantial level of residual disease. Furthermore, in FcgRIIB-/- mice lacking Yaa, IRF5-deficiency also markedly reduced disease manifestations, indicating that the beneficial effects of IRF5 deficiency in FcgRIIB-/-Yaa mice are not due only to inhibition of the enhanced TLR7 signaling associated with the Yaa mutation. Overall, we demonstrate that IRF5 plays an essential role in lupus pathogenesis in murine models and that this is mediated through pathways beyond that of type I interferon production. The fact that even IRF5 heterozygous mice developed minimal disease makes IRF5 a particularly attractive therapeutic target. Serum samples from a total of 70 mice were run on the Utz Lab Whole Protein Autoantigen Array V1.0 (a single-color platform) in order to profile their autoantibodies against a library of autoimmune antigens. All samples were run once with no replicates. The samples consisted of the following groups: For data appearing in Figure 3D, illustrating that mice lacking IRF5 have their autoantibody levels significantly affected: R2Yaa IRF5+/+: 12 R2Yaa IRF5+/-: 11 R2Yaa IRF5-/-: 14 C57BL/6 ("WT" control): 13 Total mice (arrays) for this group: 50 For data appearing in Figure 6D, illustrating that mice lacking Ifnar1 do not have their autoantibody levels significantly affected: R2Yaa Ifnar+/+: 10 R2Yaa Ifnar-/-: 10 Total mice (arrays) for this group: 20
2009-09-09 | E-GEOD-17926 | biostudies-arrayexpress
Project description:Polymorphisms in the transcription factor interferon regulatory factor 5 (IRF5) are strongly associated in human genetic studies with an increased risk of developing the autoimmune disease systemic lupus erythematosus. However, the biological role of IRF5 in lupus pathogenesis, if any, is not known. In this study we show that IRF5 is absolutely required for disease development in the FcgRIIB-/-Yaa and FcgRIIB-/- lupus models. In contrast to IRF5-sufficient FcgRIIB-/-Yaa mice, IRF5-deficient FcgRIIB-/-Yaa mice do not develop lupus manifestations and have a phenotype comparable to wildtype mice. Strikingly, full expression of IRF5 is required for the development of autoimmunity, as IRF5-heterozygotes had dramatically reduced disease. One effect of IRF5 is to induce the production of the type I interferon IFN-gamma, a cytokine implicated in lupus pathogenesis. To address the mechanism by which IRF5 promotes disease, we evaluated FcgRIIB-/-Yaa mice lacking the type I interferon receptor IFNAR1. Unlike the IRF5-deficient and IRF5-heterozygous FcgRIIB-/-Yaa mice, IFNAR1-deficient FcgRIIB-/-Yaa mice maintained a substantial level of residual disease. Furthermore, in FcgRIIB-/- mice lacking Yaa, IRF5-deficiency also markedly reduced disease manifestations, indicating that the beneficial effects of IRF5 deficiency in FcgRIIB-/-Yaa mice are not due only to inhibition of the enhanced TLR7 signaling associated with the Yaa mutation. Overall, we demonstrate that IRF5 plays an essential role in lupus pathogenesis in murine models and that this is mediated through pathways beyond that of type I interferon production. The fact that even IRF5 heterozygous mice developed minimal disease makes IRF5 a particularly attractive therapeutic target.
2009-09-09 | GSE17926 | GEO
Project description:- transcription factor interferon regulatory factor 4 (IRF4) = crucial transcription factor for different immune cells, incl pro-inflammatory Th17 and anti-inflammatory Treg cells
- IRF4 is essential for the cell differentiation and fate determination
- however molecular mechanisms of IRF4-mediated gene expression in fully differentiated Th17/Treg cells are still not fully understood
- integration of data derived from affinity-purification and full mass spectrometry-based proteome analysis with chromatin immune precipitation sequencing (ChIP-Seq)
- characterization of proteins generally involved in the T cell development as well as subtype-specific differentiation and identification of novel, yet uncharted IRF4 interactors
2024-08-02 | PXD044298 | JPOST Repository
Project description:Type I interferons (IFN-I) are critical in antimicrobial and antitumor defense. Although IFN-I signal via the interferon-stimulated gene factor 3 (ISGF3) complex consisting of STAT1, STAT2 and IRF9, IFN-I can mediate significant biological effects via ISGF3-independent pathways. For example, absence of STAT1, STAT2 or IRF9 exacerbates neurological disease in transgenic mice with CNS-production of IFN-gamma. Here we determined the role of IFN-I-driven, ISGF3-independent signaling in regulating global gene expression in STAT1, STAT2 or IRF9-deficient murine mixed glial cell cultures (MGCs). Compared with WT, the expression of IFN-gamma-stimulated genes (ISGs) was reduced in number and magnitude in MGCs that lacked STAT1, STAT2 or IRF9. There were significantly fewer ISGs in the absence of STAT1 or STAT2 versus the absence of IRF9. The majority of ISGs regulated in the STAT1-, STAT2- or IRF9-deficient MGCs individually were shared with WT. However, only a minor number of ISGs were common to WT, STAT1-, STAT2- and IRF9-deficient MGCs. While signal pathway activation in response to IFN-gamma was rapid and transient in WT MGCs, this was delayed and prolonged and correlated with increased numbers of ISGs expressed at 12 h versus 4 h IFN-gamma exposure in all three IFN-I-signaling-deficient MGCs. In conclusion, (1) IFN-I can mediate ISG expression in MGCs via ISGF3-independent signaling pathways but with reduced efficiency, with delayed and prolonged kinetics and is more dependent on STAT1 and STAT2 than IRF9, and (2) signaling pathways not involving STAT1, STAT2 or IRF9 play a minor role only in mediating ISG expression in MGCs.
2017-02-15 | E-MTAB-5445 | biostudies-arrayexpress