E-MEXP-2248
Ontology highlight
ABSTRACT:
PROVIDER: E-MEXP-2248 | ExpressionAtlas | 2015-10-22
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Rb null embryos exhibit defective fetal liver erythropoiesis. We used microarrays to compare Wt and Rb null fetal livers and to analyse gene expression differences which accompany and may underlie Rb null fetal liver degeneration, erythroid failure, and erythropoietic island dissolution. We used microarrays to compare Wt and Rb null fetal livers and analyse gene expression changes which accompany and may underlie fetal liver. Keywords: retinoblastoma, fetal liver, erythroblast, macrophage, cell death
2007-06-05 | GSE6787 | GEO
Project description:Rb null embryos exhibit defective fetal liver erythropoiesis. We used microarrays to compare Wt and Rb null fetal livers and to analyse gene expression differences which accompany and may underlie Rb null fetal liver degeneration, erythroid failure, and erythropoietic island dissolution. We used microarrays to compare Wt and Rb null fetal livers and analyse gene expression changes which accompany and may underlie fetal liver. Experiment Overall Design: Wild type and Rb null embryos were sacrificed at e12.5 and fetal livers were dissected for RNA extraction. Three embryos of each genotype were analysed.
2008-06-15 | E-GEOD-6787 | biostudies-arrayexpress
Project description:To identify p45 target genes, we conducted gene expression profiling with p45-null megakaryocytes cultured from E14.5 fetal liver. Many genes encoding membrane proteins and enzymes related to platelet function, including Txas, Glycoprotein 6 (Gp6) and Selectin P (Selp), were repressed in the absence of p45. Considering the similar DNA binding specificity of p45 and Nrf2 in vitro, we expected p45 to activate cytoprotective genes that are established Nrf2 targets. However, the expression of numerous detoxifying enzymes and stress-responsive genes, including NAD(P)H:quinone oxidoreductase (Nqo1), were increased in the absence of p45. To obtain wild type and p45-null fetal livers, p45+/- mice were crossed. Whole livers were recovered from mouse fetuses at E14.5 and single cell suspensions were prepared by successive passage through 25-gauge needles. Fetal liver cells were maintained in RPMI1640 (Wako) supplemented with 20% charcoal-stripped fetal bovine serum, 50 units/ml penicillin, 50 µg/ml streptomycin, and 50 ng/ml of recombinant human thrombopoietin. CD41+ cells were selected from a 4 day primary culture of E14.5 fetal liver cells using a MACS magnetic system (Miltenyi Biotec). The fetal liver culture with TPO described above was incubated with FITC-conjugated anti-CD41 antibody (BD Pharmingen, clone MWReg30) followed by incubation with anti-FITC microbeads. Subsequently, the microbeads were selected magnetically through MACS large cell columns (Miltenyi Biotec). Total RNA was extracted from the CD41+ cells using Isogen (Nippon Gene).
2010-03-22 | E-GEOD-15581 | biostudies-arrayexpress
Project description:DS children have a 500-fold increased risk for developing acute megakaryoblastic leukemia (AMKL). Around 10% of DS newborns have a transient myeloproliferative disorder (TMD) that resolves spontaneously. Somatic mutations acquired during fetal hematopoiesis in the GATA1 transcription factor are detected in megakaryoblasts from all the DS TMDs or AMKLs. GATA1 is an X chromosome transcription factor essential for the development of multiple hematopoietic lineages. Loss of GATA1 results in embryonic lethality due to severe anemia. The GATA1 mutations result in the expression of a shorter isoform, GATA1s. Replacement of GATA1 with GATA1s causes transient proliferation of immature fetal megakaryocytic progenitors. The Hsa21 ETS transcription factor, ERG, is expressed in megakaryocytes and erythrocytes and is involved in several types of cancer. Mutation in GATA1 gene leading to expression of the short isoform (GATA1s) that occurs on the background of trisomy 21 is regarded as one of the driving forces for megakaryocytic expansion observed in DS fetal livers. ERG, which is located on chromosome 21, is considered one of the leading candidates to cooperate with GATA1 mutation in the generation of DS AMKL. To study the in vivo cooperation between ERG and GATA1 isoforms, we crossed the ERG transgenic mice with the GATA1s Knock-in mice (GATA null background). We found that males expressing both ERG and the short isoform of GATA1(GATA1s) died in uterus between embryonic days E121/2 and E141/2.We studied erythropoiesis and megakaryopoiesis in fetal livers from the different genotypes generated from our cross. We used expression array to study the specific interaction of ERG with the different GATA1 isoforms in fetal livers from E121/2 and E141/2 and identify ERG, GATA1 and GATA1s target genes by comparing sets of genes that are activated or repressed in the presence of ERG and the two isoforms of GATA1.
2013-12-31 | E-GEOD-46481 | biostudies-arrayexpress
Project description:Deletion of the NMD component UPF2 in fetal liver. Upf2flox/+ females were mated to Upf2flox/+; Alfp-Cre males. Fetal livers were isolated from Upf2+/+; Alfp-Cre (WT) and Upf2flox/flox; AlfpCre (UPF2 null) E16.5 and E18.5 embryos.
2010-06-17 | E-MEXP-2248 | biostudies-arrayexpress
Project description:Transcription profiling of livers of adult UPF2 null mice in response to partial hepatechtomy
2015-10-22 | E-MEXP-2249 | ExpressionAtlas
Project description:DS children have a 500-fold increased risk for developing acute megakaryoblastic leukemia (AMKL). Around 10% of DS newborns have a transient myeloproliferative disorder (TMD) that resolves spontaneously. Somatic mutations acquired during fetal hematopoiesis in the GATA1 transcription factor are detected in megakaryoblasts from all the DS TMDs or AMKLs. GATA1 is an X chromosome transcription factor essential for the development of multiple hematopoietic lineages. Loss of GATA1 results in embryonic lethality due to severe anemia. The GATA1 mutations result in the expression of a shorter isoform, GATA1s. Replacement of GATA1 with GATA1s causes transient proliferation of immature fetal megakaryocytic progenitors. The Hsa21 ETS transcription factor, ERG, is expressed in megakaryocytes and erythrocytes and is involved in several types of cancer. Mutation in GATA1 gene leading to expression of the short isoform (GATA1s) that occurs on the background of trisomy 21 is regarded as one of the driving forces for megakaryocytic expansion observed in DS fetal livers. ERG, which is located on chromosome 21, is considered one of the leading candidates to cooperate with GATA1 mutation in the generation of DS AMKL. To study the in vivo cooperation between ERG and GATA1 isoforms, we crossed the ERG transgenic mice with the GATA1s Knock-in mice (GATA null background). We found that males expressing both ERG and the short isoform of GATA1(GATA1s) died in uterus between embryonic days E121/2 and E141/2.We studied erythropoiesis and megakaryopoiesis in fetal livers from the different genotypes generated from our cross.
2013-12-31 | GSE46481 | GEO
Project description:Adult and fetal hematopoietic stem cells (HSCs) display a glycolytic phenotype, which is required for maintenance of stemness; however, whether mitochondrial respiration is required to maintain HSC function is not known. Here we report that loss of the mitochondrial complex III subunit Rieske iron sulfur protein (RISP) in fetal mouse HSCs allows them to proliferate but impairs their differentiation, resulting in anemia and prenatal death. RISP null fetal HSCs displayed impaired respiration resulting in a decreased NAD+/NADH ratio. RISP null fetal HSCs and progenitors exhibited an increase in both DNA and histone methylation concomitant with increases in 2-hydroxyglutarate (2-HG), a metabolite known to inhibit DNA and histone demethylases. RISP inactivation in adult HSCs also impaired respiration resulting in loss of quiescence resulting in severe pancytopenia and lethality. Thus, respiration is dispensable for adult or fetal HSC proliferation, but essential for fetal HSC differentiation and maintenance of adult HSC quiescence.
2017-09-13 | PXD006054 | Pride
Project description:Expression profiling by array in livers of Nrf2 null mice administered CDDO-IM
| PRJNA238225 | ENA
Project description:Gene Profiling in the Livers of Wild-Type and PPARalpha-Null Mice Exposed to Perfluorooctanoic Acid (PFOA)
| PRJNA103737 | ENA