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IFIT2 mediates IFN signaling

ABSTRACT: IFit2 is highly induced in response to type I and type II interferons, dsRNA, LPS, viral and bacterial infections and it is als found in several chronic diseases.A possible role for the protein in cell proliferation, virion assembly/transport and microtubule dynamices was described. This study focus on IFIT2 proinflammatory cytokine response which might be involved in the development of septic shock. In the IFIT2 knockout mice gene expression levels before and after OVA challenge were analysed. Total RNA obtained from 3-4 male mutant mice (challenged/un-challenged) was compared to 4 wild type controls (challenged/unchallenged).

ORGANISM(S): Mus musculus

SUBMITTER: Marion Horsch

PROVIDER: E-GEOD-39953 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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IFIT2 mediates IFN signaling

Project description:IFit2 is highly induced in response to type I and type II interferons, dsRNA, LPS, viral and bacterial infections and it is als found in several chronic diseases.A possible role for the protein in cell proliferation, virion assembly/transport and microtubule dynamices was described. This study focus on IFIT2 proinflammatory cytokine response which might be involved in the development of septic shock. In the IFIT2 knockout mice gene expression levels before and after OVA challenge were analysed.

2014-05-02 | GSE39953 | GEO

Transcriptome analysis of Cox4-2 knockout mice after OVA challenge

Project description:Cytochrome c oxidase (COX) is a 13-subunit enzyme that is a key complex of the oxidative phosphorylation system of the mitochondria, which generates the vast majority of the energy of the cell.COX subunit IV is the largest nuclear-encode subunit with important regulatory functions concerning energy metabolism. COX4-2 has been knocked out. Our study indicated strong expression of Cox4-2 in lung and therefore we test this mutant line under OVA-challenge conditions expecting a new asthma mouse model. Total RNA obtained from 1/2 lung of 4 female mice of each analysed group (widltype, wildtype challenged, mutant, mutant challenged)

2015-07-15 | E-GEOD-49694 | biostudies-arrayexpress

Transcriptome analysis of Prdm11 knockout mice after OVA challenge

Project description:PRDM family members encode for progeins functionally associated with the control of cell proliferation, differentiation as well as apoptosis action in cell and tissue-specific menner. As important factors in maintenance and differentiation of human and mouse ES cells several PRDM family members were identified. Prdm11 has and outsider position within the PRDM family due to the lack of zinc-finger domains. However, a zic-finger binding motive i present and likely assue the function of protein-protein interactionl. Prdm11 was described as a candidate for tumor suppresser. However, the function of this gene is still unknown. Our study give evidence a new functional association of Prdm11 in allergic disease and asthma. Total RNA obtained from 1/2 lung of 4 female mice of each analysed group (widltype, wildtype challenged, mutant, mutant challenged)

2015-07-15 | E-GEOD-49705 | biostudies-arrayexpress

Decrease of Parkin and CD36 expression and body weight correlate with an increase of non-esterified fatty acids in a mouse model for TDP-43 pathology

Project description:TDP-43-coding mutations are found among ALS patients. In oder to express human mutant TDP-43 protein in the mouse under the control of the endogenous Tardp promoter, we have generate a mouse line wit 300% elevated TDP-43 level. Total RNA obtained from 4-6 male mutant mice was compared to 4-6 wild type controls.

2014-05-21 | E-GEOD-39585 | biostudies-arrayexpress

Genome-wide expression profiling analysis of a SMC6 mutant mouse model

Project description:The function of the SMC5-6 complex is less clear, but it has an important role in a variety of different DNA repair processes and in resolving recombination structures. Interestingly mutation at a highly conserved residue (Ser994) in the ATP hydrolysis motif in the SMC6 C-terminal domain, resulted in mice with a mild phenotype. Total RNA obtained from homozygote 4 male mutant mice was compared to 2-4 wild type or 2 heterozygote controls.

2013-04-22 | E-GEOD-38737 | biostudies-arrayexpress

Genome-wide expression profiling analysis of a Sphingomyelin Synthase 1 mutant mouse model

Project description:Lysosomal storage diseases are congenital lipid metabolism disorders, often accompaning by male infertility. Sms1, the enzyme, that generates sphingomyelin from ceramides seems to be involved in spermatogeneis and spermiogenesis. Therefore, testis but also muscle and brain of a mouse line carrying an insertional mutation in Sms1 were analysed. Total RNA obtained from 4 male mutant mice was compared to four wild type controls.

2013-01-01 | E-GEOD-37359 | biostudies-arrayexpress

Cancerous inhibitor of Protein Phosphatase 2A is a novel cell-autonomous regulator governing both T-and B-cell activation in vivo

Project description:The generation of optimal immune response requires combined activation of both T- and B-cells. Here, we demonstrate that the cancerous inhibitor of protein phosphatase 2A (CIP2A) is a novel factor that governs activation of both T- and B-cells in vivo. Upon ovalbumin challenge, CIP2A-deficient (CIP2AHOZ) mice show impaired immune response. Furthermore, CIP2AHOZ mice had impaired clearance of Listeria Monocytogenesis (L.m.) infection, combined with decreased numbers of CD8+ T-cells and IFN-? secretion. In an ovalbumin model of allergic asthma, CIP2AHOZ B-cells were impaired in IgE and IgG secretion, despite of normal Th2 differentiation and unaffected numbers of inflammatory cells or cytokines in bronchoalveolar lavage. Importantly, the cell-autonomous effect of CIP2A deficiency for both T- and B-cell activation was confirmed by in vitro assays. During the T-cell activation CIP2A, was shown to promote expression of ETS-1, whereas in B-cells CIP2A loss resulted in inhibition of MYC-mediated gene expression. Together these results identify CIP2A as a novel cell-autonomous regulator governing both T- and B-cell activation in vivo. They also identify CIP2AHOZ as a novel murine model for investigation of impaired immune response and allergic asthma. Total RNA obtained from 4 male mutant mice was compared to 4 wild type controls.

2015-06-10 | E-GEOD-56401 | biostudies-arrayexpress

Mice lacking DUF1220 protein domains are hyperactive and show reduced fecundity

Project description:Sequences encoding DUF1220 protein domains show the most extreme human lineage-specific copy number increase of any coding region in the genome and have been linked to human brain evolution. In addition, DUF1220 copy number (dosage) has been implicated in influencing brain size within the human species, both in normal populations and in individuals associated with brain size pathologies (1q21-associated microcephaly and macrocephaly). More recently, increasing dosage of a subtype of DUF1220 has been linked with increasing severity of the primary symptoms of autism. Despite these intriguing associations, a function for these domains has not been described. As a first step in addressing this question we have developed the first transgenic model of DUF1220 function by removing the single DUF1220 domain (the ancestral form) encoded in the mouse genome. While resulting DUF1220-minus (KO) mice show no obvious anatomical peculiarities, they exhibit a significantly reduced fecundity (χ2= 19.1, df = 2, p = 7.0 x 10-5). Further extensive phenotypic analyses suggest that DUF1220 KO mice are hyperactive (p < 0.05) relative to wild type litter mates. The linking of DUF1220 loss to a hyperactive phenotype is consistent with separate findings in which DUF1220 over expression results in a down-regulation of mitochondrial function, suggesting a possible role in the prolongation of developmental processes (neoteny) that is most pronounced in the human lineage. Total RNA obtained from brain of 3 male homozygous Duf1220 ko and 4 male wildtype mice

2014-09-22 | E-GEOD-58308 | biostudies-arrayexpress

Restless Legs Syndrome-associated variant in MEIS1 confers altered gene expression in embryonic ganglionic eminences

Project description:Genome-wide association studies (GWASs) identified the MEIS1 locus for Restless Legs Syndrome (RLS), but causal single nucleotide polymorphisms (SNPs) and the functional relevance have remained to be elucidated. The MEIS1 locus contains an exceptionally large number of highly conserved non-coding regions (HCNRs), which potentially function as cis-regulatory modules. We analyzed the HCNRs in the RLS-associated linkage disequilibrium (LD) block for allele-dependent enhancer activity in both zebrafish and mouse, comparing the protective and risk alleles of RLS-associated common variants. We found one enhancer, harboring the lead SNP rs12469063, which showed an allele-dependent reduction of reporter gene expression exclusively in the embryonic ganglionic eminences at developmental stage E12.5. Notably, the reporter activity overlapped with the endogenous telencephalic Meis1 expression domain, which co-localized with transcripts of all four validated RLS loci. Thus, the developing telencephalon represents the first neuroanatomic region implicated for RLS based on GWAS findings. Total RNA obtained from 2-3 male and female mice E12.5 (wildtype, heterzygote, homozygote) and 3-4 male heterozygote and wildtype mice (adult)

2014-01-29 | E-GEOD-44592 | biostudies-arrayexpress

Genome-wide expression profiling analysis of the Ali35 mutant mouseline carrying a mutation in the Shc2 gene

Project description:Analysis of changes on gene expression levels in brain and bone for the linkage to phenotypical alterations found in behavior, neurology, nociception, bone remodelling and development. Total RNA isolated from bone and brain of Ali35 mutant mice compared to wildtype controls

2014-09-01 | E-GEOD-34079 | biostudies-arrayexpress

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