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E-CBIL-21 - Transcription profiling of pancreatic islets in wild type and Tcf-1 knock-out mice to identify target genes Tcf-1 that may be responsible of mediating beta cell growth

Released on 27 February 2007, last updated on 2 June 2014
Mus musculus
Samples (100)
Arrays (2)
Protocols (7)
Mutations in several transcription factors lead to a subtype of type 2 diabetes called maturity-onset diabetes of the young (MODY), which are characterized by autosomal dominant inheritance, an early age of disease onset, and development of marked hyperglycemia with a progressive impairment in insulin secretion (Shih and Stoffel, 2002). The most frequent form of MODY is caused by mutations in the gene encoding hepatocyte nuclear factor-1a (HNF-1a, TCF1). Mutant mice with loss of Tcf1 function as well as transgenic mice expressing a naturally occurring dominant-negative form of human TCF1(P291fsinsC) in pancreatic beta cells develop progressive hyperglycemia due to impaired glucose-stimulated insulin secretion (Hagenfeldt-Johansson et al., 2001; Yamagata et al., 2002). Importantly, these mice exhibit a progressive reduction in beta cell number, proliferation rate, and pancreatic insulin content. These data indicate that Tcf-1 target genes are also required for maintenance of normal beta cell mass. In this study we sought to identify target genes of Tcf-1 that may be responsible of mediating beta cell growth by comparing gene expression profiles of Tcf-1 knock-out and wild-type littermates in isolated pancreatic islets.
Experiment types
transcription profiling by array, genetic modification
Investigation descriptionE-CBIL-21.idf.txt
Sample and data relationshipE-CBIL-21.sdrf.txt
Processed data (1)
Experiment designE-CBIL-21.biosamples.png, E-CBIL-21.biosamples.svg
Array designsA-AFFY-6.adf.txt, A-AFFY-7.adf.txt