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PubMed · 3857073

Decrease in protein C in L-asparaginase-treated patients.

J Conard·M H Horellou·P Van Dreden·F Potevin·R Zittoun·M Samama
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Antithrombin IIIAsparaginaseEnzyme-Linked Immunosorbent AssayGlycoproteinsHumansLeukemia, LymphoidProtein CLetter

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J Conard, M H Horellou, P Van Dreden, F Potevin, R Zittoun, M Samama. 1985. Decrease in protein C in L-asparaginase-treated patients.. https://doi.org/10.1111/j.1365-2141.1985.tb07368.x

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PubMed1992

Two new nonsense mutations in type Ia antithrombin III deficiency at Leu 140 and Arg 197.

Using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and DNA sequencing, the molecular basis of hereditary type Ia antithrombin III (AT III) deficiency was disclosed in two families. One mutation was a change from T to A in the codon of TTA for Leu 140 forming a stop codon of TAA, which was confirmed by mutated primer-mediated PCR-HindIII digestion. The application of this method demonstrated that all four affected members had the mutant allele in a heterozygous state and that none of unaffected subjects had this mutation. Another mutation in the second family was a change from C to T in the codon of CGA for Arg 197 also forming a stop codon of TGA, which was confirmed by PCR-HaeIII digestion. Based on these, it was concluded that the two new nonsense mutations in the AT III gene in a heterozygous state are the molecular basis of hereditary type Ia AT III deficiency.

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