First Author | Azuma K | Year | 2014 |
Journal | PLoS One | Volume | 9 |
Issue | 2 | Pages | e88643 |
PubMed ID | 24520408 | Mgi Jnum | J:212951 |
Mgi Id | MGI:5582566 | Doi | 10.1371/journal.pone.0088643 |
Citation | Azuma K, et al. (2014) Liver-specific gamma-glutamyl carboxylase-deficient mice display bleeding diathesis and short life span. PLoS One 9(2):e88643 |
abstractText | Vitamin K is a fat-soluble vitamin that plays important roles in blood coagulation and bone metabolism. One of its functions is as a co-factor for gamma-glutamyl carboxylase (Ggcx). Conventional knockout of Ggcx causes death shortly after birth in homozygous mice. We created Ggcx-floxed mice by inserting loxP sequences at the sites flanking exon 6 of Ggcx. By mating these mice with albumin-Cre mice, we generated Ggcx-deficient mice specifically in hepatocytes (Ggcx(Deltaliver/Deltaliver) mice). In contrast to conventional Ggcx knockout mice, Ggcx(Deltaliver/Deltaliver) mice had very low activity of Ggcx in the liver and survived several weeks after birth. Furthermore, compared with heterozygous mice (Ggcx(+/Deltaliver) ), Ggcx(Deltaliver/Deltaliver) mice had shorter life spans. Ggcx(Deltaliver/Deltaliver) mice displayed bleeding diathesis, which was accompanied by decreased activity of coagulation factors II and IX. Ggcx-floxed mice can prove useful in examining Ggcx functions in vivo. |