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

ABSTRACT: 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 m

INSTRUMENT(S): Affymetrix Fluidics Station 400

ORGANISM(S): Mus musculus

SUBMITTER: Markus Stoffel 

PROVIDER: E-CBIL-21 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress