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from CD99 high expressors but membranes from CD99 low expressors required exposure of 5 minutes before the 32 kD band was apparent [50]. Unfortunately, these tests gave no information about the Xga protein because the position of the Xga band was masked by the antibody light chain which became labelled. However, a 32 kD band was seen in the Xga-immunoprecipitate from Xg(a+) but not from Xg(a-) cells [50]. It has not yet been proved that this is the CD99 protein because this band was not stained by immunoblotting Xga-immunoprecipitates with 12E7. The luciferin-enhanced luminescent proceedure to detect the avidin-biotin label is very much more sensitive than immunoblotting. Our results support the theory that Xga and CD99 may be associated in the membrane. Cloning of the XG gene will increase our understanding of this relationship. The important blood group genes have been cloned but two big problems remain, regulation on antigen expression and the function of blood group polymorphisms. Rare phenotypes should still be studied because they will contribute to unravelling the mechanisms responsible for the polymorphisms. The wealth of serological information which continues to increase includes many examples of variable expression of red cell antigens. Some antigens do not show the same variation on other cells suggesting that some modes of regulation may be limited to red cells. Association of blood group antigens with proteins of known function and identification of red cell antigens on cells other than red cells will contibute to understanding the functions of the blood group polymorphisms. REFERENCES 1. P.L. Mollison, C.P. Engelfreit and M. Contreras, Blood Transfusion in Clinical Medicine. Blackwell Scientfic Publications, Oxford (1993). 2. M. Lewis (Chairman) et al, Vox Sang., 61_, 158-160 (1991). 3. G.L. Daniels, J.J. Moulds (chairman) et al, Vox Sang., 65, 77-80 (1993). 4. A.C. Petty, J. Immunol. Meth., 161. 91-95 (1993). 5. J. M. Moulds, in Immunobiology of Transfusion Medicine. G. Garratty ed. Marcel Dekker. Inc., New York, (1994) pp. 273-297. 6. J.M. Moulds, M.W. Nickells, J.J. Moulds, M.C. Brown and J.P. Atkinson, J. Exp. Med., 173, 1159-1163 (1991). 7. N. Rao, D.J. Ferguson, S-F. Lee and M.J. Telen, J. Immun., 146, 3502-3507 (1991). 8. A.C. Petty, (abs) Transfusion Medicine 3 Suppl 1, 84 (1993). 9. J.M. Moulds, J.J. Moulds, M. Brown and J.P. Atkinson, Vox Sang. 62, 230-235 (1992).
DOI link for from CD99 high expressors but membranes from CD99 low expressors required exposure of 5 minutes before the 32 kD band was apparent [50]. Unfortunately, these tests gave no information about the Xga protein because the position of the Xga band was masked by the antibody light chain which became labelled. However, a 32 kD band was seen in the Xga-immunoprecipitate from Xg(a+) but not from Xg(a-) cells [50]. It has not yet been proved that this is the CD99 protein because this band was not stained by immunoblotting Xga-immunoprecipitates with 12E7. The luciferin-enhanced luminescent proceedure to detect the avidin-biotin label is very much more sensitive than immunoblotting. Our results support the theory that Xga and CD99 may be associated in the membrane. Cloning of the XG gene will increase our understanding of this relationship. The important blood group genes have been cloned but two big problems remain, regulation on antigen expression and the function of blood group polymorphisms. Rare phenotypes should still be studied because they will contribute to unravelling the mechanisms responsible for the polymorphisms. The wealth of serological information which continues to increase includes many examples of variable expression of red cell antigens. Some antigens do not show the same variation on other cells suggesting that some modes of regulation may be limited to red cells. Association of blood group antigens with proteins of known function and identification of red cell antigens on cells other than red cells will contibute to understanding the functions of the blood group polymorphisms. REFERENCES 1. P.L. Mollison, C.P. Engelfreit and M. Contreras, Blood Transfusion in Clinical Medicine. Blackwell Scientfic Publications, Oxford (1993). 2. M. Lewis (Chairman) et al, Vox Sang., 61_, 158-160 (1991). 3. G.L. Daniels, J.J. Moulds (chairman) et al, Vox Sang., 65, 77-80 (1993). 4. A.C. Petty, J. Immunol. Meth., 161. 91-95 (1993). 5. J. M. Moulds, in Immunobiology of Transfusion Medicine. G. Garratty ed. Marcel Dekker. Inc., New York, (1994) pp. 273-297. 6. J.M. Moulds, M.W. Nickells, J.J. Moulds, M.C. Brown and J.P. Atkinson, J. Exp. Med., 173, 1159-1163 (1991). 7. N. Rao, D.J. Ferguson, S-F. Lee and M.J. Telen, J. Immun., 146, 3502-3507 (1991). 8. A.C. Petty, (abs) Transfusion Medicine 3 Suppl 1, 84 (1993). 9. J.M. Moulds, J.J. Moulds, M. Brown and J.P. Atkinson, Vox Sang. 62, 230-235 (1992).
from CD99 high expressors but membranes from CD99 low expressors required exposure of 5 minutes before the 32 kD band was apparent [50]. Unfortunately, these tests gave no information about the Xga protein because the position of the Xga band was masked by the antibody light chain which became labelled. However, a 32 kD band was seen in the Xga-immunoprecipitate from Xg(a+) but not from Xg(a-) cells [50]. It has not yet been proved that this is the CD99 protein because this band was not stained by immunoblotting Xga-immunoprecipitates with 12E7. The luciferin-enhanced luminescent proceedure to detect the avidin-biotin label is very much more sensitive than immunoblotting. Our results support the theory that Xga and CD99 may be associated in the membrane. Cloning of the XG gene will increase our understanding of this relationship. The important blood group genes have been cloned but two big problems remain, regulation on antigen expression and the function of blood group polymorphisms. Rare phenotypes should still be studied because they will contribute to unravelling the mechanisms responsible for the polymorphisms. The wealth of serological information which continues to increase includes many examples of variable expression of red cell antigens. Some antigens do not show the same variation on other cells suggesting that some modes of regulation may be limited to red cells. Association of blood group antigens with proteins of known function and identification of red cell antigens on cells other than red cells will contibute to understanding the functions of the blood group polymorphisms. REFERENCES 1. P.L. Mollison, C.P. Engelfreit and M. Contreras, Blood Transfusion in Clinical Medicine. Blackwell Scientfic Publications, Oxford (1993). 2. M. Lewis (Chairman) et al, Vox Sang., 61_, 158-160 (1991). 3. G.L. Daniels, J.J. Moulds (chairman) et al, Vox Sang., 65, 77-80 (1993). 4. A.C. Petty, J. Immunol. Meth., 161. 91-95 (1993). 5. J. M. Moulds, in Immunobiology of Transfusion Medicine. G. Garratty ed. Marcel Dekker. Inc., New York, (1994) pp. 273-297. 6. J.M. Moulds, M.W. Nickells, J.J. Moulds, M.C. Brown and J.P. Atkinson, J. Exp. Med., 173, 1159-1163 (1991). 7. N. Rao, D.J. Ferguson, S-F. Lee and M.J. Telen, J. Immun., 146, 3502-3507 (1991). 8. A.C. Petty, (abs) Transfusion Medicine 3 Suppl 1, 84 (1993). 9. J.M. Moulds, J.J. Moulds, M. Brown and J.P. Atkinson, Vox Sang. 62, 230-235 (1992).
ABSTRACT