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E-CBIL-37 - Transcription profiling of wild type and foxA1 null mice

Released on 12 September 2007, last updated on 1 May 2014
Mus musculus
Samples (5)
Array (1)
Protocols (8)
The aim of this experiment was to use microarray analysis to examine the phenotype of the foxA1 (HNF3alpha) null mouse. foxA1 has a central role in the regulatory control of islet genes essential for glucose homeostasis in vivo. Previous studies have shown that the foxA1 null mouse demonstrates severe postnatal growth retardation followed by death between P2 and P12. These mutant mice are hypoglycemic despite unchanged expression of foxA1 target genes involved in hepatic gluconeogenesis. foxA1 is known to bind to and transactivate the proglucagon gene promoter and mice null for this gene have a 70% reduction in pancreatic proglucagon gene expression and plasma glucagon levels are reduced markedly. Marco Vatamaniuk from Klaus Kaestner Lab extracted RNA from isolated islets. Three biological replicates were provided for both the WT and Null.
Experiment types
transcription profiling by array, dye swap, genetic modification
Functional genomics of the beta-cell: SCHAD regulates insulin secretion independent of K+ currents. Hardy O.T., Hohmeier H.E., Becker T.C., Manduchi E., Doliba N.M., Gupta R.K., White P., Stoeckert C.J. Jr., Matschinsky F.M., Newgard C.B., Kaestner K.H. Mol Endocrinol  (2006)
Investigation descriptionE-CBIL-37.idf.txt
Sample and data relationshipE-CBIL-37.sdrf.txt
Raw data (1)
Processed data (1)
Experiment designE-CBIL-37.biosamples.png, E-CBIL-37.biosamples.svg
Array designA-CBIL-2.adf.txt