Fig. 5.
Fig. 5. Nucleotide sequence analyses. / (A) Nucleotide sequence analysis of amplified GPIIIa cDNA derived from an Oea (−) individual (HPA-1b/1b) and the Oea (+) (HPA-1b/1b) grandfather. PCR products encompassing bases 56-698 (left panel) and bases 1666-2415 (right panel) were subcloned into the plasmid vector pGEM-5Zf and sequenced. The missing of the triplet AAG (underlined) in Oea (+) individual results in ΔLys611. Both individuals carry the Pro33 GPIIIa form, which corresponds to their HPA-1b phenotypes. (B) Nucleotide sequence analysis of amplified GPIIIa DNA derived from Oea (+) and Oea (−) individuals. PCR products encompassing the entire exon 10 were sequenced directly. The mutated GPIIIa allele of Oea (+) individual is shown by the asterisks (top panel). The deletion of the triplet AAG (underlined) resulting in a shift of 3 bases was observed in Oea (+), but not in Oea (−) individual (bottom panel).

Nucleotide sequence analyses.

(A) Nucleotide sequence analysis of amplified GPIIIa cDNA derived from an Oea (−) individual (HPA-1b/1b) and the Oea (+) (HPA-1b/1b) grandfather. PCR products encompassing bases 56-698 (left panel) and bases 1666-2415 (right panel) were subcloned into the plasmid vector pGEM-5Zf and sequenced. The missing of the triplet AAG (underlined) in Oea (+) individual results in ΔLys611. Both individuals carry the Pro33 GPIIIa form, which corresponds to their HPA-1b phenotypes. (B) Nucleotide sequence analysis of amplified GPIIIa DNA derived from Oea (+) and Oea (−) individuals. PCR products encompassing the entire exon 10 were sequenced directly. The mutated GPIIIa allele of Oea (+) individual is shown by the asterisks (top panel). The deletion of the triplet AAG (underlined) resulting in a shift of 3 bases was observed in Oea (+), but not in Oea (−) individual (bottom panel).

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