Info

154 bp 154 bp

Jka Jk"

97 bp 97 bp

Jka Jk"

97 bp 97 bp

Fig. 3. Kidd genotyping by ASPCR. (A) Schematic of polymorphisms associated with normal/null and JKA and JKB Kidd alleles. (B) Products of each analysis are run sets of four ordered as follows: the JKA (nt838G) reaction, the JKB (nt838A) reaction, the Kidd normal (exon 6 nt-1G) reaction, and the Kidd null (exon 6 nt-1A) reaction. Allele-specific amplification of either JKA or JKB generates a 97-bp product, and allele-specific amplification of the intron 5 product generates a 154-bp product. A 423-bp HGH internal positive control product is detected in each reaction possessing DNA template. Set A: Analysis of a Caucasian JKA/JKA homozygote; set B: Analysis of a Caucasian JKB/JKB homozygote; set C: Analysis of a Polynesian Jk(a-b-) individual. Fifteen to 20 ||L of each amplified PCR product was analyzed by electrophoresis through 2% agarose gels and stained with ethidium bromide.

Fig. 3. Kidd genotyping by ASPCR. (A) Schematic of polymorphisms associated with normal/null and JKA and JKB Kidd alleles. (B) Products of each analysis are run sets of four ordered as follows: the JKA (nt838G) reaction, the JKB (nt838A) reaction, the Kidd normal (exon 6 nt-1G) reaction, and the Kidd null (exon 6 nt-1A) reaction. Allele-specific amplification of either JKA or JKB generates a 97-bp product, and allele-specific amplification of the intron 5 product generates a 154-bp product. A 423-bp HGH internal positive control product is detected in each reaction possessing DNA template. Set A: Analysis of a Caucasian JKA/JKA homozygote; set B: Analysis of a Caucasian JKB/JKB homozygote; set C: Analysis of a Polynesian Jk(a-b-) individual. Fifteen to 20 ||L of each amplified PCR product was analyzed by electrophoresis through 2% agarose gels and stained with ethidium bromide.

not available. All Polynesian Jk(a-b-) individuals (n = 10) typed were homozygous for a silent JKB allele possessing the intron 5 G^A 3' splice acceptor mutation (69). Irshaid et al. reported the absence of any mutations associated with silent JK alleles among 64 Swedish Caucasians and detection of 8 intron 5 heterozygotes among 46 Polynesians (63). Together, these limited results indicate that the silent Polynesian JK allele, based on its low frequency, is unlikely to cause false positives when conducting prenatal genotyping of individuals from non-Polynesian groups; however, the risk of potential misinterpretation of genotyping results must be considered, especially because this mutation has been observed as the molecular basis of the Jk(a-b-) phenotype in a single Chinese-American (68). The existence of this rare allele again highlights the importance of establishing concordance between the parental genotypes and serotypes prior to predicting the fetal serotype based on genotyping results.

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