Abstract
We performed cDNA microarrays (Affymetrix Mouse Gene 1.0 ST Chip) to analyze the transcriptome of hematopoietic stem and progenitor cells (HSPCs) from E15.5dpc wild type and Geminin (Gmnn) knockout embryos. Lineage negative cells from embryonic livers were isolated using fluorescence activated cell sorting. RNA samples were used to examine the transcriptional programs regulated by Geminin during embryonic hematopoiesis. The data sets were analyzed using the GeneSpring v12.5 platform (Agilent). The list of differentially expressed genes was filtered in meta-analyses to investigate the molecular basis of the phenotype observed in the knockout embryos, which exhibited defective hematopoiesis and death. The data from this study are related to the research article “Geminin deletion increases the number of fetal hematopoietic stem cells by affecting the expression of key transcription factors” (Karamitros et al., 2015) [1].The microarray dataset has been deposited at the Gene Expression Omnibus (GEO) under accession GEO: GSE53056.
Highlights
We performed cDNA microarrays (Affymetrix Mouse Gene 1.0 ST Chip) to analyze the transcriptome of hematopoietic stem and progenitor cells (HSPCs) from E15.5dpc wild type and Geminin (Gmnn) knockout embryos
Control and Geminin knockout littermate embryos were utilized in order to examine the role of Geminin in the developing mouse hematopoietic system. Control were those embryos whose genotype had both Geminin alleles intact, whereas both alleles were disrupted/absent in the Gemininfl/ko Vav1:iCre counterparts in a tissue-specific manner [1,2]
The transcriptome of both groups was examined by means of cDNA microarrays and differentially expressed genes are presented as fold change of knockout versus control expression levels
Summary
Figure (clustering), graph, table cDNA microarrays using GPL6246 [MoGene-1_0-st] Affymetrix Mouse Gene 1.0 ST Array [transcript (gene) version]. The list of differentially expressed genes includes changes in transcription factors and epigenetic regulators that can link Geminin, a cell cycle inhibitor, with novel cellular pathways. This dataset can serve as a reference point for various studies pertaining to hematopoietic cell lineage commitment/differentiation and hematopoietic malignancies. Control were those embryos whose genotype had both Geminin alleles intact, whereas both alleles were disrupted/absent in the Gemininfl/ko Vav1:iCre counterparts in a tissue-specific manner [1,2] The transcriptome of both groups was examined by means of cDNA microarrays and differentially expressed genes are presented as fold change of knockout versus control expression levels. Direct link to deposited files. http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc 1⁄4GSE53056
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