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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bock, S. C. Articles by Prochownik, E. V. Search for Related Content PubMed PubMed Citation Articles by Bock, S. C. Articles by Prochownik, E. V. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Molecular genetic survey of 16 kindreds with hereditary antithrombin III deficiency SC Bock and EV Prochownik Rockefeller University, New York. Molecular genetic techniques were utilized to examine antithrombin III (ATIII) gene status in 16 independently ascertained kindreds with hereditary ATIII deficiency. In one of these families antithrombin III deficiency is caused by hemizygosity of the ATIII locus. In the remaining 15 kindreds, two copies of the ATIII gene are present and appear to be grossly normal at the level of whole genome Southern blotting, suggesting that small deletions, insertions or limited nucleotide substitution(s) in the antithrombin III gene, or "trans- acting" defects at other loci involved in the processing, modification, and secretion of biologically active ATIII are responsible for the observed anticoagulant disorders. Volume 70, Issue 5, pp. 1273-1278, 11/01/1987 Copyright © 1987 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. Robbins, M. Forrest, and D. Royston Hypercoagulable States Seminars in Cardiothoracic and Vascular Anesthesia, November 1, 1997; 1(4): 295 - 318. [Abstract] [PDF]

	Copyright © 1987 by American Society of Hematology         Online ISSN: 1528-0020