E-MEXP-2248
Ontology highlight
ABSTRACT:
PROVIDER: E-MEXP-2248 | ExpressionAtlas | 2015-10-22
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MEXP-2248-analysis-methods.tsv | Tabular | |||
| E-MEXP-2248-atlasExperimentSummary.Rdata | Rdata | |||
| E-MEXP-2248-configuration.xml | Xml | |||
| E-MEXP-2248-percentile-ranks.tsv | Tabular | |||
| E-MEXP-2248.condensed-sdrf.tsv | Tabular |
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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: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.
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Project description:Expression profiling by array in livers of Nrf2 null mice administered CDDO-IM
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Project description:The cAMP response element binding protein (Creb) is a member of a leucine zipper transcription factor family that regulates gene expression primarily in response to the intracellular cAMP signalling pathway. Previous studies have shown Creb1-null mice suffer respiratory failure with lung atelectasis and a large reduction in Sftpd mRNA. Using a new line of Creb1-null mice we have further investigated Creb function in the developing mouse lung, focussing on differentiation of the airway epithelium. The lungs of Creb1-null fetal mice showed normal respiratory development until E17.5 when proximal and distal airways fail to inflate. Subsequent ultrastructural analysis of the lungs of E17.5 Creb1-null fetal mice revealed a defect in AEC differentiation with a reduction in proportions of type-II AECs and in particular, a very large reduction in type-I AECs. Furthermore, immunostaining for the proximal epithelial cell markers Scgb1a1 (also known as CC10) (Clara cells), Foxj1 (Ciliated cells), and CGRP (Neuroendocrine cells) showed delayed or defective proximal epithelial differentiation in Creb1-null fetal lungs. Quantitative real time PCR (qRT-PCR) analysis at E17.5 in Creb1-null fetal lungs showed differential expression of mRNAs for Creb/Atf1 subfamily members, surfactant-associated proteins, type-I AEC markers and proximal epithelial markers. Furthermore, whole-genome microarray analysis at E17.5 in Creb1-null fetal lungs has provided novel genes which will prove useful to further investigate Creb-mediated signalling in lung development. Together these results demonstrate that Creb plays a key role in determining cell lineages and differentiation of the developing lung epithelium.
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