E-GEOD-59140 - SIRT1 deficiency enhances RA induced mESC differentiation

Released on 21 August 2014, last updated on 22 August 2014
Mus musculus
Samples (16)
Array (1)
Protocols (7)
Retinoid homeostasis is critical for normal embryonic development, and both the deficiency and excess of these compounds are associated with congenital malformations. Here we found that SIRT1, the most conserved mammalian NAD+-dependent deacetylase, contributes to the maintenance of homeostatic retinoic acid (RA) signaling and modulates mouse embryonic stem cell (mESC) differentiation. Our data show that SIRT1 deficiency enhances RA signaling, thereby accelerating mES cell differentiation in response to RA. Our findings highlight the importance of SIRT1 in transcriptional regulation of ESC pluripotency and embryogenesis. Three pairs of sh-Control and sh-SIRT1 E14 mESC cells (with dulpicate for each sample) were treated with vehicle ethanol or with 20 nM of RA for 2 days. Total RNA was isolated using a Qiagen RNA easy mini kit with on-column DNAseI treatment. RNA quality was validated with the Agilent 2100 Bioanalyzer in the microarray facility. Three-pairs of ethanol treated samples, and 4 RA treated sh-Control, and 6 RA treated sh-SIRT1 samples were analyzed by Agilent Whole Mouse Genome 4x44 formate oligo arrays (014868) (Agilent Technologies) following the Agilent 1-color microarray-based gene expression analysis protocol.
Experiment type
transcription profiling by array 
Investigation descriptionE-GEOD-59140.idf.txt
Sample and data relationshipE-GEOD-59140.sdrf.txt
Raw data (1)E-GEOD-59140.raw.1.zip
Processed data (1)E-GEOD-59140.processed.1.zip
Array designA-AGIL-28.adf.txt