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186 results on '"Zelinski, T."'

13. International Society of Blood Transfusion Working Party on red cell immunogenetics and blood group terminology: Cancun report (2012)

Author

Storry, J. R., primary, Castilho, L., additional, Daniels, G., additional, Flegel, W. A., additional, Garratty, G., additional, de Haas, M., additional, Hyland, C., additional, Lomas-Francis, C., additional, Moulds, J. M., additional, Nogues, N., additional, Olsson, M. L., additional, Poole, J., additional, Reid, M. E., additional, Rouger, P., additional, van der Schoot, E., additional, Scott, M., additional, Tani, Y., additional, Yu, L.-C., additional, Wendel, S., additional, Westhoff, C., additional, Yahalom, V., additional, and Zelinski, T., additional

Published
2013
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16. Mutation at codon 322 in the human acetylcholinesterase (ACHE) gene accounts for YT blood group polymorphism

Author

Bartels, C F, Zelinski, T, and Lockridge, O

Subjects
Isoantigens, Erythrocytes, Polymorphism, Genetic, Base Sequence, Genotype, DNA Mutational Analysis, Molecular Sequence Data, Exons, Polymerase Chain Reaction, Acetylcholinesterase, Blood Group Antigens, Humans, Point Mutation, Amino Acid Sequence, Oligonucleotide Probes, Chromosomes, Human, Pair 7, Research Article
Abstract

Acetylcholinesterase is present in innervated tissues, where its function is to terminate nerve impulse transmission. It is also found in the red blood cell membrane, where its function is unknown. We report the first genetic variant of human acetylcholinesterase and support the identity of acetylcholinesterase as the YT blood group antigen. DNA sequencing shows that the wild-type sequence of acetylcholinesterase with His322 (CAC) is the YT1 blood group antigen and that the rare variant of acetylcholinesterase with Asn322 (AAC) is the YT2 blood group antigen. Two additional point mutations in the acetylcholinesterase gene do not affect the amino acid sequence of the mature enzyme.

Published
1993

19. Terminology for Red Cell Surface Antigens

Author

Daniels, G.L., primary, Anstee, D.J., additional, Cartron, J.P., additional, Dahr, W., additional, Garratty, G., additional, Henry, S., additional, Jorgensen, J., additional, Judd, W.J., additional, Kornstad, L., additional, Levene, C., additional, Lomas‐Francis, C., additional, Lubenko, A., additional, Moulds, J.J., additional, Moulds, J.M., additional, Moulds, M., additional, Overbeeke, M., additional, Reid, M.E., additional, Rouger, P., additional, Scott, M., additional, Seidl, S., additional, Sistonen, P., additional, Tani, Y., additional, Wendel, S., additional, and Zelinski, T., additional

Published
1999
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24. Terminology for Red Cell Surface Antigens. Makuhari Report

Author

Daniels, G.L., primary, Anstee, D.J., additional, Cartron, J. P., additional, Dahr, W., additional, Henry, S., additional, Issitt, P.D., additional, Jorgensen, J., additional, Judd, W.J., additional, Kornstad, L., additional, Levene, C., additional, Lomas-Francis, C., additional, Lubenko, A., additional, Mallory, D., additional, Moulds, J. M., additional, Moulds, J. J., additional, Okubo, Y., additional, Overbeeke, M., additional, Reid, M. E., additional, Rouger, P., additional, Seidl, S., additional, Sistonen, P., additional, Wendel, S., additional, and Zelinski, T., additional

Published
1996
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26. Blood Group Terminology 1995: ISBT Working Party on Terminology for Red Cell Surface Antigens

Author

Daniels, G. L., primary, Anstee, D. J., additional, Cartron, J. P., additional, Dahr, W., additional, Jørgensen, J., additional, Kornstad, L., additional, Levene, C., additional, Lomas-Francis, C., additional, Lubenko, A., additional, Mallory, D., additional, Moulds, J. J., additional, Okubo, Y., additional, Overbeeke, M., additional, Reid, M. E., additional, Rouger, P., additional, Seidl, S., additional, Sistonen, P., additional, Wendel, S., additional, Woodfield, G., additional, and Zelinski, T., additional

Published
1995
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32. ISBT Working Party on Terminology for Red Cell Surface Antigens: São Paulo Report

Author

Daniels, G. L., primary, Moulds, J. J., additional, Anstee, D. J., additional, Bird, G. W. G., additional, Brodheim, E., additional, Cartron, J.-P., additional, Dahr, W., additional, Engelfriet, C. P., additional, Issitt, P. D., additional, Jørgensen, J., additional, Kornstad, L., additional, Lewis, M., additional, Levene, C., additional, Lubenko, A., additional, Mallory, D., additional, Morel, P., additional, Nordhagen, R., additional, Okubo, Y., additional, Reid, M., additional, Rouger, Ph., additional, Salmon, Ch., additional, Seidl, S., additional, Sistonen, P., additional, Wendel, S., additional, Woodfield, G., additional, and Zelinski, T., additional

Published
1993
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34. INTERNATIONAL SOCIETY OF BLOOD TRANSFUSION SOCIÉTÉ INTERNATIONALE DE TRANSFUSION SANGUINE: ISBT Working Party on Terminology for Red Cell Surface Antigens: Los Angeles Report

Author

Lewis, M., primary, Anstee, D.J., additional, Bird, G. W. G., additional, Brodheim, E., additional, Cartron, J.-P., additional, Contreras, M., additional, Dahr, W., additional, Daniels, G. L., additional, Engelfriet, C. P., additional, Issitt, P. D., additional, Jørgensen, J., additional, Kornstad, L., additional, Lubenko, A., additional, McCreary, J., additional, Morel, P., additional, Moulds, J. J., additional, Nevanlinna, H., additional, Nordhagen, R., additional, Okubo, Y., additional, Pehta, J., additional, Rouger, Ph., additional, Rubinstein, P., additional, Salmon, Ch., additional, Seidl, S., additional, Sistonen, P., additional, Tippett, P., additional, Walker, R. H., additional, Woodfield, G., additional, Young, S., additional, and Zelinski, T., additional

Published
1991
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42. Chromosome location of genes encoding human blood groups

Author

Reid, M.E., McManus, K., and Zelinski, T.

Abstract

The chromosomal locations of genes controlling the expression of some 200 antigens constituting the 23 established human blood group systems have been reviewed. Twenty-one of the these genes are located on 12 autosomes, and two are located on the X chromosome. Refined chromosomal positions, to a single cytogenetically distinguishable band, have been established for 13 of the 23 genes. For the remainder, continued investigation will achieve the same result. The genes (RD, MER2, and OK) controlling the expression of one low-incidence and two high-incidence erythrocyte antigens have also been presented. Of these, OK is the most likely candidate for blood group system status, because its chromosomal location distinguishes it from all established system genes except LE and LW, and, the product of the OK gene is different from those of LE and LW (Table 3). This issue will be considered at the next meeting (scheduled for July 1998) of the ISBT Working Party. Alternatively, RD and MER2 are not good candidates for blood group system status because RD and MER2 reside in chromosomal regions containing genes for other blood group systems. In addition, the products of RD and SC have similar biochemical characteristics, ^3^3 and the product of MER2 has not yet been defined (Table 3). The challenge remaining for blood group scientists is characterization of genes that control expression of the approximately 50 other known erythrocyte antigens. Most of these are members of the ISBT's 700 (low-incidence) or 901 (high-incidence) series.^1^3 Because the current genetic information for each of these antigens (attained by serologic investigation) varies considerably, future studies will have to rely on ''tools'' from related disciplines to provide the additional information. Use of resources such as molecular biological protocols and GBD should facilitate the effort.

Published
1998
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43. Choline regulates phosphatidylethanolamine biosynthesis in isolated hamster heart.

Author

Zelinski, T A and Choy, P C

Abstract

The effect of choline on phosphatidylethanolamine biosynthesis in the isolated hamster heart was investigated. Hamster hearts were perfused with [2-14C]ethanolamine in the presence of 0-0.5 mM choline. Incorporation of label into phosphatidylethanolamine was decreased 28% at 0.2-0.5 mM choline. Analysis of the ethanolamine-containing metabolites of the CDP-ethanolamine pathway revealed that choline (0.2-0.5 mM) in the perfusate had no effect on the labeling of ethanolamine. However, a 28-30% reduction in the labeling of phosphoethanolamine and CDP-ethanolamine was observed. Concurrently, there was a 2-fold increase in the intracellular choline level. Although the formation of CDP-ethanolamine is regarded as the rate-limiting step for phosphatidylethanolamine biosynthesis, choline was found to inhibit ethanolamine kinase, but did not have any effect on phosphoethanolamine cytidylyltransferase. Hence, choline may provide an additional mechanism for the regulation of phosphatidylethanolamine biosynthesis.

Published
1982
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50. The ELO Blood Group Polymorphism Is Located in the Putative First Extracellular Loop of Human Erythrocyte Band 3

Author

Zelinski, T., Punter, F., McManus, K., and Coghlan, G.

Abstract

AbstractBackground and Objectives: The low incidence red cell antigen ELO (700.51) has been excluded from 13 of 23 established blood group systems. Information relative to the Diego system has not been reported. To investigate a possible association between ELO and the gene controlling Diego blood group polymorphisms, we undertook molecular studies of AE1 (anion exchanger 1 gene). Materials and Methods: DNA from a family segregating for ELO and from the original ELO proposita was amplified by PCR using intronic primers flanking exons 11–20 of AE1. Subsequently, single-strand conformational polymorphism (SSCP) analysis and DNA sequencing were conducted. Results: We have observed an exon 12 SSCP in all ELO+ individuals tested. This SSCP is the result of a C→T mutation in exon 12 of AE1 which leads to an Arg432→Trp amino acid substitution in the putative first extracellular loop of band 3 and thereby accounts for the Diego blood group system polymorphism known as ELO. Conclusions: In light of these findings, the International Society of Blood Transfusion Working Party on Terminology for Red Cell Surface Antigens has designated ELO as a member of the Diego blood group system (010008 or DI8) and rendered the previous numerical designation (700.51) obsolete.

Published
1998

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