Fig. 2.
Fig. 2. Pedigree of family B-a with the Taq I-A and Taq I-B alleles associated with the mutations exon 1: −8 (g → c) and exon 12: 10590 (Del C), respectively. Patients B-a1, B-a3, and B-a5 did not show any strong thrombotic symptoms. Patient B-a2 suffered from a superficial thrombophelitis during her pregnancy. (A) Pedigree and sequence of the single basepair deletion. Solid symbols, carriers of the Taq I-A allele/exon 1:−8 (g → c); hatched symbols, carriers of the Taq I-B allele/exon 12: 10590(Del C). (B) Coagulation parameters. (C) Comparison of wild-type and mutated sequences. (D) Fluorescence sequence analysis of wild-type exon 12 PCR products. (E) Analysis of an individual B-a1. Mutated and wild-type exon 12 sequences are superimposed. The arrow indicates the deletion of a single base at nucleotide position 10590.

Pedigree of family B-a with the Taq I-A and Taq I-B alleles associated with the mutations exon 1: −8 (g → c) and exon 12: 10590 (Del C), respectively. Patients B-a1, B-a3, and B-a5 did not show any strong thrombotic symptoms. Patient B-a2 suffered from a superficial thrombophelitis during her pregnancy. (A) Pedigree and sequence of the single basepair deletion. Solid symbols, carriers of the Taq I-A allele/exon 1:−8 (g → c); hatched symbols, carriers of the Taq I-B allele/exon 12: 10590(Del C). (B) Coagulation parameters. (C) Comparison of wild-type and mutated sequences. (D) Fluorescence sequence analysis of wild-type exon 12 PCR products. (E) Analysis of an individual B-a1. Mutated and wild-type exon 12 sequences are superimposed. The arrow indicates the deletion of a single base at nucleotide position 10590.

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