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<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="GSM469866"><item key="GENOME/VARIATION">wild type</item></item></item><item><item key="GSM469866"><item key="GENOME/VARIATION">wild type</item></item></item><item><item key="GSM469866"><item key="GENOME/VARIATION">wild type</item></item></item><item><item key="GSM469866"><item key="GENOME/VARIATION">wild type</item></item></item><item><item key="GSM469870"><item key="GENOME/VARIATION">Hoxd4 transgenic</item></item></item><item><item key="GSM469870"><item key="GENOME/VARIATION">Hoxd4 transgenic</item></item></item><item><item key="GSM469870"><item key="GENOME/VARIATION">Hoxd4 transgenic</item></item></item><item><item key="GSM469870"><item key="GENOME/VARIATION">Hoxd4 transgenic</item></item></item></item><item key="id">5891</item><item key="pop_total">0</item><item key="platform">6</item><item key="summary_wrapped">Homeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In...</item><item key="geo_gse_id">E-GEOD-18991</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>class</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_gds_id"/><item key="slug">overexpression-of-hoxd4-transcription-factor-alter</item><item key="geo_id_plat">E-GEOD-18991_A-AFFY-45</item><item key="name">Overexpression of Hoxd4 transcription factor alters transcriptional profiles in mouse chondrocytes at E18.5</item><item key="created">Nov.11, 2014</item><item key="summary">Homeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxd4 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform. Embryos were dissected from four different mouse litters at E18.5. Embryos from each litter were grouped according their genotype: TA=control; TR=transgenic.</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-18991</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-18991/samples/</item></data></biogps>
