| First Author | Gailani D | Year | 1997 |
| Journal | Blood Coagul Fibrinolysis | Volume | 8 |
| Issue | 2 | Pages | 134-44 |
| PubMed ID | 9518045 | Mgi Jnum | J:40270 |
| Mgi Id | MGI:87615 | Doi | 10.1097/00001721-199703000-00008 |
| Citation | Gailani D, et al. (1997) A murine model of factor XI deficiency. Blood Coagul Fibrinolysis 8(2):134-44 |
| abstractText | To facilitate investigations into the physiologic and pathologic roles of factor XI, we have developed a murine model of severe factor XI deficiency using the technique of homologous recombination in embryonic stem cells. The factor XI gene was disrupted by introducing a neomycin phosphotransferase gene into the fifth exon. The activated partial thromboplastin times of homozygous null mice were prolonged (158- > 200 s) compared with wild type (25-34 s) and heterozygous null (40-61 s) litter mates. Factor XI activity was absent from the plasma of mice homozygous for the null mutation and factor XI mRNA was undetectable by Northern blot and reverse transcription/PCR in the livers of homozygous null animals. The genotypes of progeny from matings of mice heterozygous for the factor XI null allele followed the expected Mendelian ratio (1:2:1, wild type 26%, heterozygote null 54%, homozygous null 20%), indicating that severe factor XI deficiency did not result in increased intrauterine death. Results of a tail transection bleeding time assay were similar for wild type and homozygous null animals with, at most, a tendency for slightly prolonged bleeding in the homozygous null animals. The factor XI deficient mice are a unique tool for evaluating the role of factor XI in normal hemostasis and pathologic coagulation. |
