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| Status |
Public on Apr 01, 2009 |
| Title |
Expression profile of Sall4-null ES cells and Sall4 heterozygous ES cells |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by array
|
| Summary |
Sall4 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
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| Overall design |
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 feeders
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| Citation(s) |
19350679 |
| |
| Submission date |
Dec 25, 2008 |
| Last update date |
Feb 11, 2019 |
| Contact name |
Ryuichi Nishinakamura |
| Organization name |
Kumamoto University
|
| Department |
Institute of Molecular Embryology and Genetics
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| Lab |
Kumamoto UniversityDivision of Integrative Cell Biology
|
| Street address |
2-2-1 Honjo
|
| City |
Kumamoto |
| ZIP/Postal code |
860-0811 |
| Country |
Japan |
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| Platforms (1) |
| GPL1261 |
[Mouse430_2] Affymetrix Mouse Genome 430 2.0 Array |
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| Samples (4)
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| Relations |
| BioProject |
PRJNA111349 |
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