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Technical Briefs |
Deutsches Herzzentrum München and 1. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, Munich, Germany;
aaddress correspondence to this author at: Deutsches Herzzentrum München, Lazarettstrasse 36, D-80636 Munich, Germany; fax 49-89-1218-3053, e-mail wkoch@dhm.mhn.de
| The first 20% of the full text of this article appears below. |
Intron 16 of the angiotensin I-converting enzyme gene (ACE) contains an insertion/deletion (I/D) polymorphism that is characterized by the presence (I allele) or absence (D allele) of a 289-bp incomplete alu type repeat sequence (1)(2). The D allele has been related to higher concentrations of ACE mRNA in cells and increased ACE concentration and activity in plasma and serum (1)(3)(4)(5)(6). There is great continuing interest in the link between the ACE I/D polymorphism and interindividual variations in physiologic properties and disease susceptibility. Reported associations include physical activity and endurance, drug response, and neuropathologic, cardiac, and cardiovascular diseases (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20). However, a considerable number of findings are in disagreement with the existence of such relationships (21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31), and more work is required before the role of the ACE I/D polymorphism in health and disease can be firmly established.
Conventional genotyping of the ACE I/D polymorphism involves PCR, using primers that flank the insertion sequence, and exploits the different migration velocities of I- and D-allelespecific PCR products during electrophoresis in gel matrices (32). Here we describe an assay for genotyping of the ACE I/D polymorphism that is based on the TaqMan technique (33). The TaqMan
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