P
Pieter H. Reitsma
Researcher at Leiden University
Publications - 288
Citations - 29623
Pieter H. Reitsma is an academic researcher from Leiden University. The author has contributed to research in topics: Gene & Venous thrombosis. The author has an hindex of 76, co-authored 287 publications receiving 28728 citations. Previous affiliations of Pieter H. Reitsma include Washington University in St. Louis & Leiden University Medical Center.
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Journal ArticleDOI
Characterization of mini-protein S, a recombinant variant of protein S that lacks the sex hormone binding globulin-like domain.
M. Van Wijnen,J. G. Stam,G. T. G. Chang,Joost C. M. Meijers,Pieter H. Reitsma,Rogier M. Bertina,Bonno N. Bouma +6 more
TL;DR: A recombinant protein S molecule is constructed that fails to bind C4BP and still displays cofactor activity for APC, and it is demonstrated that N-terminal residues 1-242 are sufficient for the expression of APC co Factor activity in a system using purified components.
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Intron-exon organization of the human gene coding for the lipoprotein-associated coagulation inhibitor: the factor Xa dependent inhibitor of the extrinsic pathway of coagulation.
TL;DR: The cloning of the human LACI gene is reported and the elucidation of its intron-exon organization is reported, which shows that the domain structure of other Kunitz-type protease inhibitors is reflected in the intron and exon organization of the gene.
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Preschool Phonological Representations and Development of Reading Skills
TL;DR: This article found that individual differences in the quality of phonological representations play an important role in the development of explicit phonological awareness and reading acquisition in preschoolers. But, the results of the three longitudinal studies provided inconclusive support for the theory that individuals differences in their own phonological representation play a significant role in their reading development.
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Partial protein S gene deletion in a family with hereditary thrombophilia
TL;DR: Using Southern blotting on probands of six unrelated families with hereditary protein S deficiency, one proband was found to have a grossly abnormal gene pattern, which agrees with the notion that hereditary thrombophilia associated withprotein S deficiency is indeed directly the result of a defect in the protein S gene.
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Mutations in severe, type III von Willebrand's disease in the Dutch population: candidate missense and nonsense mutations associated with reduced levels of von Willebrand factor messenger RNA.
TL;DR: The von Willebrand factor (vWF) genes of nine unrelated, severe, type III vonWillebrand's disease (vWD) patients and four unrelated Dutch type I vWD patients were screened for mutations in exons that contain CGA codons, which are liable to mutation to TGA stop codons.