<?xml version="1.0" encoding="ASCII"?>
<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="ownerprofile_id">arrayexpress_sid</item><item key="species">mouse</item><item key="factors"><item><item key="GSM451590"><item key="genotype">wild type</item></item></item><item><item key="GSM451590"><item key="genotype">wild type</item></item></item><item><item key="GSM451590"><item key="genotype">wild type</item></item></item><item><item key="GSM451590"><item key="genotype">wild type</item></item></item><item><item key="GSM451594"><item key="genotype">Crebbp+/-</item></item></item><item><item key="GSM451594"><item key="genotype">Crebbp+/-</item></item></item><item><item key="GSM451594"><item key="genotype">Crebbp+/-</item></item></item><item><item key="GSM451594"><item key="genotype">Crebbp+/-</item></item></item></item><item key="id">5824</item><item key="pop_total">0</item><item key="platform">6</item><item key="summary_wrapped">Myelodysplastic syndrome (MDS) is considered a disease of hematopoietic stem cell (HSC) origin.  To begin to unravel the molecular...</item><item key="pubmed_id">22198154</item><item key="geo_gse_id">E-GEOD-18061</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">1</item><item key="sample_count">8</item><item key="tags"><item>bone</item><item>bone marrow</item><item>cell</item><item>disease</item><item>hematopoietic system</item><item>liver</item><item>myelodysplastic syndrome</item><item>stem cell</item><item>syndrome</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_gds_id"/><item key="slug">transcription-profiling-by-array-of-hematopoietic</item><item key="geo_id_plat">E-GEOD-18061_A-AFFY-45</item><item key="name">Transcription profiling by array of hematopoietic stem cells from mice heterozygous for CREB binding protein</item><item key="created">Nov.11, 2014</item><item key="summary">Myelodysplastic syndrome (MDS) is considered a disease of hematopoietic stem cell (HSC) origin.  To begin to unravel the molecular mechanisms underlying the deregulation of HSCs in MDS, we performed comparative gene expression profiling on Crebbp+/- and wild type HSCs.  We chose to isolate HSCs from the fetal liver (FLHSC) because at this stage there were no differences in cell number between Crebbp+/- and wild type fetal livers, suggesting no overt hematopoietic differences.  Thus, any change in gene expression found in Crebbp+/- FLHSCs is likely to reflect the initially compromised genetic program of HSC regulation, as opposed to that of Crebbp+/- HSCs in adult bone marrow, where secondary changes in gene expression may also occur as compensatory mechanisms for a compromised or failing hematopoietic system. We used day 14.5 post coitus FLHSC (Sca-1+,Lin-,AA4.1+,c-Kit++) from wild type (wt) and Crebbp heterozygous (ht) embryos to examine changes in gene expression before overt myelodysplastic disease manifestation. Total RNA from wt and Crebbp+/- FLHSCs was isolated, PCR-amplified using the Ovation RNA amplification system and hybridized to Affymetrix Mouse 430 2.0 expression microarrays.</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-18061</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-18061/samples/</item></data></biogps>
