Molecular basis for the high-incidence antigens of the Kell blood group system

Transfusion ◽  
1997 ◽  
Vol 37 (11-12) ◽  
pp. 1117-1122 ◽  
Author(s):  
S Lee ◽  
DS Naime ◽  
ME Reid ◽  
CM Redman
Transfusion ◽  
2003 ◽  
Vol 35 (10) ◽  
pp. 822-825 ◽  
Author(s):  
S. Lee ◽  
X. Wu ◽  
M. Reid ◽  
C. Redman

Vox Sanguinis ◽  
2011 ◽  
Vol 102 (2) ◽  
pp. 167-170 ◽  
Author(s):  
C. H. Hipsky ◽  
K. Hue-Roye ◽  
C. Lomas-Francis ◽  
C.-H. Huang ◽  
M. E. Reid

2002 ◽  
Vol 277 (48) ◽  
pp. 45854-45859 ◽  
Author(s):  
Nathalie Roudier ◽  
Pierre Ripoche ◽  
Pierre Gane ◽  
Pierre Yves Le Pennec ◽  
Geoff Daniels ◽  
...  

Transfusion ◽  
2006 ◽  
Vol 46 (8) ◽  
pp. 1323-1327 ◽  
Author(s):  
Soohee Lee ◽  
Asim K. Debnath ◽  
Xu Wu ◽  
Terry Scofield ◽  
Terry George ◽  
...  

Blood ◽  
1991 ◽  
Vol 78 (6) ◽  
pp. 1603-1606 ◽  
Author(s):  
MJ Telen ◽  
C Le Van Kim ◽  
A Chung ◽  
JP Cartron ◽  
Y Colin

Abstract Glycophorin C (GPC) and glycophorin D (GPD) are highly glycosylated integral membrane proteins of human erythrocytes encoded by the same gene and associated with expression of Gerbich blood group system antigens. GPC/D deficiency (the Leach phenotype) is a rare condition usually found after identification of Gerbich blood group system antibodies in persons undergoing prenatal or pretransfusion evaluation. In all cases, the Leach phenotype has been associated with elliptocytosis. Characterization of the molecular basis of this phenotype in three previously uninvestigated families has shown that the most common genetic basis of GPC/D deficiency is deletion of exons 3 and 4 of the GPC gene. However, in one family, the Leach phenotype appeared due to a deletion of one nucleotide in exon 3, causing a frameshift mutation in the messenger RNA and premature generation of a stop codon. The GPC and GPD protein sequences are therefore interrupted in the extracellular domain and probably intracellularly degraded.


Blood ◽  
1957 ◽  
Vol 12 (2) ◽  
pp. 115-122 ◽  
Author(s):  
MIGUEL LAYRISSE ◽  
TULIO ARENDS

Abstract The distribution of the Diego factor has been studied in various Mongoloid, Caucasian and Negroid populations. In six South American Indian stocks, one Canadian Indian stock and two groups of Asiatic Mongoloids it was present in high incidence. In Caucasians tested, negative results were found. In two groups of Venezuelan Negroes with probable Indian admixture the factor was also present. The Diego antigen was inherited in single dose (heterozygous) in 41 families studied and could be followed through several generations with no sex-linkage. The first samples of anti-Diego serum reacted only in the indirect anti-globulin test to a titer between 1:256 and 1:512. The enzymes papain and trypsin gave no advantage. It is more active at room temperature (25 C. and 37 C.) than at cold temperature (4 C. and 18 C.). The most suitable pH range is from 5.0 to 8.0. The Diego factor can be considered as part of a new blood group system (the Diego system) which could be classified as the tenth firmly established blood system.


Transfusion ◽  
2013 ◽  
pp. n/a-n/a ◽  
Author(s):  
Randall W. Velliquette ◽  
Kim Hue-Roye ◽  
Christine Lomas-Francis ◽  
Barbara Gillen ◽  
Jennifer Schierts ◽  
...  

2015 ◽  
Vol 9 (1) ◽  
pp. 48 ◽  
Author(s):  
RoziHanisa Musa ◽  
NorAsiah Muhamad ◽  
Afifah Hassan ◽  
Yasmin Ayob ◽  
NarazahMohd Yusoff

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