The mutation was identified as G>A substitution in exon 14, resulting in a nonconservative substitution of glycine by aspartic acid at amino acid 745 (p.G745D; p.G494D in exon 9 in the C57BL/6J strain (which has a 5-exon 251aa deletion)). Western blot analysis demonstrated that expressed protein was present in pancreatic islets of homozygous mice. (J:108421)