| First Author | Wang L | Year | 1997 |
| Journal | Proc Natl Acad Sci U S A | Volume | 94 |
| Issue | 21 | Pages | 11563-6 |
| PubMed ID | 9326649 | Mgi Jnum | J:43590 |
| Mgi Id | MGI:1098077 | Doi | 10.1073/pnas.94.21.11563 |
| Citation | Wang L, et al. (1997) A factor IX-deficient mouse model for hemophilia B gene therapy. Proc Natl Acad Sci U S A 94(21):11563-6 |
| abstractText | We have generated a mouse where the clotting factor IX (FIX) gene has been disrupted by homologous recombination. The FIX nullizygous (-/-) mouse was devoid of factor IX antigen in plasma, Consistent with the bleeding disorder, the factor IX coagulant activities for wild-type (+/+), heterozygous (+/-), and homozygous (-/-) mice were 92%, 53%, and <5%, respectively, in activated partial thromboplastin time assays, Plasma factor IX activity in the deficient mice (-/-) was restored by introducing wild- type murine FIX gene via adenoviral vectors, Thus, these factor IX-deficient mice provide a useful animal model for gene therapy studies of hemophilia B. |
