Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA276077 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The goal of this study was to profile Blimp1 binding in E18.5 small intestine using a Blimp-1-eGFP knock-in allele, and to compare Blimp-1-eGFP genomic binding with Irf-1 genomic binding in normal small intestine. Changes in Irf-1 binding between wild type and Prdm1/Blimp-1 mutant small intestine were also assessed. ChIP-seq was performed for Blimp-1-eGFP in duplicate in E18.5 small intestine expressing the fusion protein using anti-GFP antibody. As a negative control a single anti-GFP ChIP was also performed in wild type small intestine. ChIP-seq for Irf-1 was performed in duplicate in both wild type and Prdm1/Blimp-1 mutant E18.5 small intestine using an anti-Irf-1 antibody. Duplicate IgG ChIP control in wild types was performed as a negative control. All samples had an associated input chromatin sample sequenced.
2015-07-10 | E-GEOD-66069 | biostudies-arrayexpress
Project description:The goal of this study was to profile Blimp1 binding in E18.5 small intestine using a Blimp-1-eGFP knock-in allele, and to compare Blimp-1-eGFP genomic binding with Irf-1 genomic binding in normal small intestine. Changes in Irf-1 binding between wild type and Prdm1/Blimp-1 mutant small intestine were also assessed.
2015-07-10 | GSE66069 | GEO
Project description:In many mammalian species, the intestinal epithelium is immature at birth. During the suckling to weaning transition, the intestine matures. This developmental transition is the result of a genetic program that is intrinsic to the gut and independent of luminal content, but its regulators have not been identified. We investigated the function of the transcriptional repressor Blimp-1 using mice with intestine-specific ablation of Blimp-1. Deletion of Blimp-1 results in growth retardation and excess neonatal mortality. Mutant mice lack all typical epithelial features of the suckling period and are born with features of adult-like intestine. To assess the function of the gene Prdm1 (Blimp) on postnatal day 7 intestinal epithelium, VillinCre-Blimpflox and control (VillinCre-Blimpwt or Cre-Blimpflox) mice were generated. Mice were sacrificed at day 7 postnatal, and pieces of whole mid-intestine were taken for analysis.
2011-07-17 | E-GEOD-30556 | biostudies-arrayexpress
Project description:Antigen-specific effector CD8+ T cells deficient in Blimp-1 (Prdm1) do not acquire maximal effector functions, evade terminal differentiation, and more rapidly acquire some hallmark properties of memory CD8+ T cells. In this study, we compared the gene expression profiles of wildtype and Prdm1-/- LCMV-specific effector CD8+ T cells to better understand the molecular mechanisms underlying this striking phenotype. DNA microarray analysis was performed of DbGP33-41 and DbNP396-404 tetramer-positive effector CD8+ T cells FACS-sorted at day 8 post-LCMV infection from four independent samples of either Blimp-1 conditional knockout mice (CKO; Blimp-1flox/flox x GranzymeB-cre+) or wildtype (WT) littermate controls.
2010-08-19 | E-GEOD-17211 | biostudies-arrayexpress
Project description:We performed microarray analysis to examine the differential gene expression profiles between Prdm1 (Blimp-1)-deleted and control keratinocytes. Keratinocytes isolated from Prdm1-floxed K5-CreER positive (CKO) mice were cultured in the presence of 4OHT to induce deletion of the Prdm1 allele in vitro. Prdm1-floxed K5-CreER positive (CKO) keratinocytes treated with the ethanol solvent control (EtOH) or Prdm1-floxed K5-CreER negative (control) keratinocytes treated with 4OHT or EtOH served as controls. Microarray analyses revealed that there were 93 genes up-regulated and 109 genes down-regulated by more than 2-fold in the CKO + 4OHT group in comparison with the CKO + EtOH, Ctrl + 4OHT or Ctrl + EtOH groups. Several corneocytes-related genes, including Rptn, Lce1f, Krt1 and Lce1d, are significantly down-regulated and several cytokines/chemokines, including Cxcl1, Cxcl2, Cxcl5 and Il24, are significantly up-regulated upon the deletion of Prdm1 in vitro. We analyzed the transcription profiles in control and Blimp-1-deficient keratinocytes using the GeneChip® Mouse Expression Array 430A.
2013-04-02 | E-GEOD-34586 | biostudies-arrayexpress
Project description:Interleukin-23 (IL-23) is a pro-inflammatory cytokine required for the pathogenicity of T helper 17 (Th17) cells but the molecular mechanisms governing this process remain unclear. We identified the transcription factor Blimp-1 (Prdm1) as a key IL-23-induced factor that drove the inflammatory function of Th17 cells. In contrast to thymic deletion of Blimp-1, which causes T cell development defects and spontaneous autoimmunity, peripheral deletion of this transcription factor resulted in reduced Th17 activation and reduced severity of autoimmune encephalomyelitis. Furthermore, genome wide occupancy and overexpression studies in Th17 cells revealed that Blimp-1 co-localized with transcription factors RORγt, STAT-3 and p300 at the Il23r, Il17a/f and Csf2 cytokine loci to enhance their expression. Blimp-1 also directly bound to and repressed cytokine loci Il2 and Bcl6. Taken together, our results demonstrate that Blimp-1 is an essential transcription factor downstream of IL-23 that acts in concert with RORγt to activate the Th17 inflammatory program. Genome-wide binding analysis of Blimp1 from in vitro generated T effector and regulatory cells
2016-06-15 | E-GEOD-75724 | biostudies-arrayexpress
Project description:In many mammalian species, the intestinal epithelium is immature at birth. During the suckling to weaning transition, the intestine matures. This developmental transition is the result of a genetic program that is intrinsic to the gut and independent of luminal content, but its regulators have not been identified. We investigated the function of the transcriptional repressor Blimp-1 using mice with intestine-specific ablation of Blimp-1. Deletion of Blimp-1 results in growth retardation and excess neonatal mortality. Mutant mice lack all typical epithelial features of the suckling period and are born with features of adult-like intestine.
2011-07-18 | GSE30556 | GEO
Project description:Antigen-specific effector CD8+ T cells deficient in Blimp-1 (Prdm1) do not acquire maximal effector functions, evade terminal differentiation, and more rapidly acquire some hallmark properties of memory CD8+ T cells. In this study, we compared the gene expression profiles of wildtype and Prdm1-/- LCMV-specific effector CD8+ T cells to better understand the molecular mechanisms underlying this striking phenotype.
2009-07-22 | GSE17211 | GEO
Project description:Using wild type and Ash1l ∆SET mutant embryonic stem cells, against a prevalent notion, here we report di-,tri-methylation of histone H3 Lys36 occur independently of ongoing transcription. Ash1l ∆SET mutant shows the impaired methylation levels in broad range of genome. Intriguingly, data implicate that a binding of retinoic acid receptor to a certain genomic region promotes installation of the tri-methylation in the retinoic acid receptor-associated gene independent of its ongoing transcription.
2013-11-20 | GSE48421 | GEO
Project description:Expression profiling of wild-type and Prdm1 null mouse trophoblast giant cell cultures using Illumina whole genome mouse V2 arrays. The hypothesis tested was that Prdm1/Blimp1 regulates expression of genes required for spiral artery trophoblast giant cell function. Prdm1 null and littermate control wild-type trophoblast stem cell clones were generated from blastocyst outgrowths. Total RNA was obtained from multiple replicates of four wild-type TS cell clones and four Prdm1 null TS cell clones differenitated for zero, two, four and six days by growth factor withdrawal and hybridized to Illumina WG6_V2 arrays
2016-03-14 | E-GEOD-74409 | biostudies-arrayexpress