ArrayExpress Uploader05585flox/-absentdelta/-absentflox/-presentdelta/-presentarrayexpress_sid6Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that...19350679E-GEOD-14219/profile/8773/arrayexpressuploader24cellfibroblastsyndromeDec.12, 2014Falseexpression-profile-of-sall4-null-es-cells-and-sallE-GEOD-14219_A-AFFY-45Expression profile of Sall4-null ES cells and Sall4 heterozygous ES cellsNov.10, 2014Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that Sall4 absence leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. However, a subsequent report indicated that shRNA-mediated Sall4 inhibition in ES cells led to a severe reduction in Oct3/4 and a secondary increase in Cdx2, which resulted in complete differentiation into the trophectoderm when cultured in the feeder-free condition. So we profiled gene expression changes when Sall4 is deleted in ES cells in the presence or absence of feeder cells. key word: embryonic stem (ES) cell, Sall4, feeder ES cells were cultured with or without mouse embryonic fibroblast (MEF) feeder cells in LIF-supplemented medium as described. To maintain the expression of Oct3/4, all ES cells were cultured in the presence of Blasticidin. Four samples were analyzed. GSM356329, GSM356330 : cultured in the absence of feeders GSM356331, GSM356332 : cultured on the feedershttp://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-14219mousehttp://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-14219/samples/