The proteins on the erythrocyte cell surface include a wide variety of different oligosaccharides that are attached in a variety of ways to the protein. However, it spite of this variation, there are many structures that are very common. One of the most typical “core” buildings is something called H-antigen. It really is made up of many different sugars but the outdoors end of the H-antigen structure always consists of a fucose (Fuc) residue, a galactose residue (Gal), and an N-acetylglucosamine (GlcNAc) residue.
14) residue to form a branched framework by the end of the oligosaccharide (see diagram below). The enzyme that catalyzes this reaction is called N-acetylaminogalactosyltransferase or A enzyme. The gene because of this enzyme is situated on chromosome 9. The OMIN (Online Mendelian Inheritance in Man) entry for the ABO bloodstream group is 110300. It contains an abundance of information on the topic. Normal red blood cells are named “self” so we don’t have antibodies against our very own cells. However, we will have antibodies against the red blood cells of other people’s bloodstream if their cell surface sugars are different from ours.
This is the basis of ABO bloodstream group and it’s why we have to match blood types in a blood transfusion. The ABO bloodstream group was discovered over a hundred years ago by Karl Landsteiner (Nobel Laureate: Karl Landsteiner). The biochemical basis was only elucidated in the 1970’s when the technology for evaluating the carbohydrate structure of glycoproteins was worked out. There’s an allele of the A enzyme gene which involves only an extremely small number of mutations but the result is to switch the enzyme from one that exchanges GalNAc to one that transfers galactose (Gal). The variant enzyme is called B enzyme (galactosyltransferase) and the B antigen structure has a terminal galactose (Gal) instead of a terminal GalNAc.
If you are homozygous for the B allele on chromosome 9 then all your red blood cells will have the B antigen oligosaccharide on their surface. You will not make antibodies from this framework because it’s “self.” Additionally you received’t have antibodies against H-antigen for the reason why described earlier. Nevertheless, you won’t recognize A antigen as self so your antibodies will attack any foreign cells that come from people with the standard wild-type allele (A). People with bloodstream type A will have antibodies against B antigen.
They can get blood from people who have O blood type but they will reject blood from people with B blood type. You now have everything you need to figure out who can give and receive blood from every possible mixture of alleles: AA, AO, AB, BO, and OO.
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There are no known natural effects of these differing blood types. People with A, B, AB and O phenotypes do not vary in fitness in any major way that people have had the opportunity to identify. This shows that the complete absence of the enzyme (null mutation) is natural in today’s human population and so is the switch from one form of the enzyme to some other.
Suggestions that bloodstream type establishes susceptibility for some infections are normal in the technological literature. Many of them have not organized. The very best correlation is a possible association between blood type susceptibility and O to cholera. The ABO alleles appear to be segregating in the human population by random genetic drift. The O allele (non-functional enzyme) is the most typical allele. The B allele is minimal because it arose more recently common-probably.
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