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<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="pop_total">0</item><item key="id">7110</item><item key="factors"><item><item key="GSM1054629"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM1054629"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM1054629"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM1054629"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM1054629"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM1054629"><item key="GENOTYPE">wild type</item></item></item><item><item key="GSM1054635"><item key="GENOTYPE">Snfl2 Ex6DEL</item></item></item><item><item key="GSM1054635"><item key="GENOTYPE">Snfl2 Ex6DEL</item></item></item><item><item key="GSM1054635"><item key="GENOTYPE">Snfl2 Ex6DEL</item></item></item><item><item key="GSM1054635"><item key="GENOTYPE">Snfl2 Ex6DEL</item></item></item><item><item key="GSM1054635"><item key="GENOTYPE">Snfl2 Ex6DEL</item></item></item><item><item key="GSM1054635"><item key="GENOTYPE">Snfl2 Ex6DEL</item></item></item></item><item key="ownerprofile_id">arrayexpress_sid</item><item key="platform">6</item><item key="summary_wrapped">We investigate the role of Snf2l in ovaries by characterizing a mouse bearing an inactivating deletion on the ATPase domain of Snf2l...</item><item key="pubmed_id">23616592</item><item key="geo_gse_id">E-GEOD-42997</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">1</item><item key="sample_count">12</item><item key="tags"><item>gonadotropin</item><item>serum</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_gds_id"/><item key="slug">the-iswi-atpase-snf2l-is-required-for-superovulati</item><item key="geo_id_plat">E-GEOD-42997_A-AFFY-45</item><item key="name">The ISWI ATPase Snf2L is required for superovulation and regulates Fgl2 in differentiating mouse granulosa cells</item><item key="created">Nov.12, 2014</item><item key="summary">We investigate the role of Snf2l in ovaries by characterizing a mouse bearing an inactivating deletion on the ATPase domain of Snf2l (Ex6DEL). Snf2l mutant mice produce significantly fewer eggs than control mice when superovulated. Thus, gonadotropin stimulation leads to a significant deficit in secondary follicles and an increase in abnormal antral follicles. We profiled the expression of granulosa cells from Snf2l WT and Ex6DEL mice treated with pregnant mares' serum gonadotropin followed by human chorionic gonadotropin Granulosa cells from either Snf2l WT or Ex6DEL mice treated with PMSG followed by hCG were collected at 0h and 4h post-hCG.  Each array includes granulosa cells pooled from 5 mice.</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-42997</item><item key="species">mouse</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-42997/samples/</item></data></biogps>
