These Tgm2t/t floxed mice possess loxP sites flanking exons 6-8 of the transglutaminase 2, C polypeptide (Tgm2) gene. The donating investigator states that the remaining frt-flanked neo cassette conveys no abnormalities. Tgm2 is a calcium-dependent enzyme that catalyzes the crosslinking of proteins. TGM2 mediates signaling by various G-protein coupled receptors and has been found to be involved in apoptosis, fibronectin stabilization, cataract development, neurodegeneration, and wound healing. TGM2 has also been cited as an autoantigen involved in celiac disease and the onset of Type 2 diabetes mellitus (T2DM). Mice that are homozygous for this allele are viable and fertile. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exons 6-8 deleted in the cre-expressing tissues.
For example, when bred to mice carrying the Tg(CMV-cre)1Cgn allele ( see Stock No. 006054), mice exhibit normal glucose tolerance, insulin sensitivity and glucose stimulated insulin secretion on a standard or high fat diet. Fibroblasts from these mice exhibit decreased adhesion. When these TGM2-deficient mice are bred to B6CBA-Tg(HDexon1)62Gpb/1J mice (Stock No. 002810), resulting offspring contain more huntingtin protein aggregates within the cerebral cortex and striatum, with no difference in the onset of motor dysfunction and the mean lifespan, compared to Tg(HDexon1)62Gpb transgenic mice.
