Literature DB >> 8430449

Polymerase chain reaction-based detection of MN blood group-specific sequences in the human genome.

V A Corfield1, J C Moolman, R Martell, P A Brink.   

Abstract

The MN blood group antigens have traditionally been detected by serotyping; however, development of a DNA-based method offers flexibility in the determination of this highly polymorphic system. Genotyping the MN blood group antigens was performed by polymerase chain reaction amplification of the specific alleles (PASA) in the human genome. In separate paired reactions, M or N allele-specific oligonucleotide primers were amplified with a common distal primer. Only in the presence of the homologous template was a 781-base pair polymerase chain reaction amplification product visible after agarose gel electrophoresis and ethidium bromide staining. This method of genotyping could be performed using either 1 microgram of extracted DNA or 0.5 microL of whole blood, and the results showed 100-percent correlation with those obtained by serotyping. PASA-based genotyping of MN blood group antigens, which requires a small amount of starting material, has application in linkage and population studies and in forensic medicine.

Entities:  

Mesh:

Substances:

Year:  1993        PMID: 8430449     DOI: 10.1046/j.1537-2995.1993.33293158042.x

Source DB:  PubMed          Journal:  Transfusion        ISSN: 0041-1132            Impact factor:   3.157


  9 in total

1.  Sequence-specific primers for MNS blood group genotyping.

Authors:  Guido A Heymann; Abdulgabar Salama
Journal:  Blood Transfus       Date:  2010-07       Impact factor: 3.443

2.  Evidence of a long QT founder gene with varying phenotypic expression in South African families.

Authors:  T de Jager; C H Corbett; J C Badenhorst; P A Brink; V A Corfield
Journal:  J Med Genet       Date:  1996-07       Impact factor: 6.318

3.  An improved method for MN genotyping by the polymerase chain reaction.

Authors:  N Nakayashiki; Y Sasaki
Journal:  Int J Legal Med       Date:  1996       Impact factor: 2.686

4.  A gene locus for progressive familial heart block type II (PFHBII) maps to chromosome 1q32.2-q32.3.

Authors:  Pedro Fernandez; Johanna Moolman-Smook; Paul Brink; Valerie Corfield
Journal:  Hum Genet       Date:  2005-10-28       Impact factor: 4.132

5.  MYBPH acts as modifier of cardiac hypertrophy in hypertrophic cardiomyopathy (HCM) patients.

Authors:  J M Mouton; L van der Merwe; A Goosen; M Revera; P A Brink; J C Moolman-Smook; C Kinnear
Journal:  Hum Genet       Date:  2016-03-11       Impact factor: 4.132

6.  The origins of hypertrophic cardiomyopathy-causing mutations in two South African subpopulations: a unique profile of both independent and founder events.

Authors:  J C Moolman-Smook; W J De Lange; E C Bruwer; P A Brink; V A Corfield
Journal:  Am J Hum Genet       Date:  1999-11       Impact factor: 11.025

7.  Clinical and prognostic evaluation of familial hypertrophic cardiomyopathy in two South African families with different cardiac beta myosin heavy chain gene mutations.

Authors:  B M Posen; J C Moolman; V A Corfield; P A Brink
Journal:  Br Heart J       Date:  1995-07

8.  Diagnostic disparity and identification of two TNNI3 gene mutations, one novel and one arising de novo, in South African patients with restrictive cardiomyopathy and focal ventricular hypertrophy.

Authors:  Jomien M Mouton; Adriano S Pellizzon; Althea Goosen; Craig J Kinnear; Philip G Herbst; Paul A Brink; Johanna C Moolman-Smook
Journal:  Cardiovasc J Afr       Date:  2015 Mar-Apr       Impact factor: 1.167

9.  AKAP9 is a genetic modifier of congenital long-QT syndrome type 1.

Authors:  Carin P de Villiers; Lize van der Merwe; Lia Crotti; Althea Goosen; Alfred L George; Peter J Schwartz; Paul A Brink; Johanna C Moolman-Smook; Valerie A Corfield
Journal:  Circ Cardiovasc Genet       Date:  2014-08-02
  9 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.