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Prepublished online as a Blood First Edition Paper on April 30, 2002; DOI 10.1182/blood-2002-01-0188. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-01-0188v1 100/4/1490    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Yu, L.-C. Articles by Lin, M. Search for Related Content PubMed PubMed Citation Articles by Yu, L.-C. Articles by Lin, M. Related Collections Transfusion Medicine Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 August 2002, Vol. 100, No. 4, pp. 1490-1492 BRIEF REPORT Molecular genetic analysis for the B3 allele Lung-Chih Yu, Yuh-Ching Twu, Ming-Lun Chou, Ching-Yi Chang, Chia-Ying Wu, and Marie Lin From the Transfusion Medicine Laboratory, Department of Medical Research, and the Immunohematology Reference Laboratory, Mackay Memorial Hospital, Taipei, Taiwan. Molecular genetic analysis of 14 samples from unrelated individuals with the B3 phenotype is reported here. Two different molecular changes in the blood group B gene were observed. One case was demonstrated to possess a 247G  T mutation, which predicts an Asp83Tyr alteration. The B genes of the other 13 cases were shown to have a G  A mutation at the +5 nucleotide of intron 3 (intervening sequence 3 [IVS3] + 5G  A). Reverse transcription polymerase chain reaction analysis showed that the complete exon 1-exon 7 B transcript was absent, and transcripts that skipped exon 3 were instead present in the RNA sample from the B3 individual with the IVS3 + 5G  A mutation. The result shows that the IVS3 + 5G  A mutation destroys the conserved sequence of the splice donor site and leads to the skipping of exon 3 during messenger RNA processing. The B3 transcript without exon 3 predicts a B-transferase product that lacks 19 amino acids in the N-terminal segment. © 2002 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: D.-P. Chen, C.-P. Tseng, H.-T. Lin, and C.-F. Sun Application of Real-Time PCR and Melting Curve Analysis in Rapid Detection of Ael and Bel Blood Types Ann. Clin. Lab. Sci., January 1, 2005; 35(1): 25 - 30. [Abstract] [Full Text] [PDF] Z.-H. Deng, Q. Yu, Y.-L. Lian, G.-G. Wu, Y.-Q. Su, and X. Zhang Identification of a Novel B Variant Allele at the ABO Locus in Chinese Han Individuals with B Subgroup Ann. Clin. Lab. Sci., January 1, 2005; 35(3): 265 - 269. [Abstract] [Full Text] [PDF] A. Seltsam, M. Hallensleben, A. Kollmann, and R. Blasczyk The nature of diversity and diversification at the ABO locus Blood, October 15, 2003; 102(8): 3035 - 3042. [Abstract] [Full Text] [PDF]

	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020