glycophorin a and b

This article incorporates text from the United States National Library of Medicine, which is in the public domain. Glycophorin A/B Antibody (5F60) is available as both the non-conjugated anti-Glycophorin A/B antibody form, as well as multiple conjugated forms of anti-Glycophorin A/B antibody, including PE. [25], Mi-IX (MNS32) occurs with a frequency of 0.43% in Denmark.[26]. [33] The erythrocyte binding antigen 175 of P. falciparum recognises the terminal Neu5Ac(alpha 2-3)Gal-sequences of glycophorin A. Natl. [provided by RefSeq, Feb 2012] [4] In chimpanzees M reacts strong but N only weakly. There are at least three variants: MD, NE and Ph. These molecules bear the antigenic determinants for the MN and Ss blood groups [122, 123]. [5], The Dantu antigen was described in 1984. S2CID 34245274. The Mi-III phenotype occurs in 6.28% of Hong Kong Chinese. Human glycophorin A belongs to a family of structurally related cell surface glycoproteins which are expressed in erythroid cells. change (a) is affected only by ligands specific for glycophorin Aand (b) results from a ligand-induced interaction between glycophorin Aandskeletal proteins. All these hybrids have glutamic acid at residue 658 of band 3, but lack the required amino acids from GPA6. This alteration in glycoslation is detectable by the presence of a new 32kDa glycoprotein stainable with PAS. (2011) analyzed nucleotide diversity of the glycophorin gene family in 15 African populations with different levels of malaria exposure. Instead, dose–response relationships have to be determined from available human in vivo data for GPA mutations where robust dose estimates are available. [7] The Dantu phenotype occurs with a frequency of Dantu phenotype is ~0.005 in American Blacks and < 0.001 in Germans.[8]. The only known platelet abnormality is the surface presence of glycophorin A, which is normally present on the erythroid lineage, on multiple cell lines capable of differentiating into megakaryocytes, and is postulated to be present on immature megakaryocytes in normal bone marrow.183 Whether this abnormality underlies the pathogenesis of this disorder or is secondary to abnormal megakaryocytopoiesis is unknown at present. GYPB gene consists of 5 exons and has 97% sequence homology with GYPA from the 5' … Heterozygous individuals carrying one M and one N allele (50% of the population) can be analyzed for mutational loss of either of these alleles using allele-specific monoclonal antibodies (reviewed in Grant and Bigbee, 1993). Proc. [13] Similar to the case of Mi-I this mutation results in a loss of the glycosylation at the asparagine26 residue. Of these, only MNSs and U are routinely typed. Also in the horse, this tissue-specific regulation of αGSU expression is documented (Farmerie et al., 1997). When AE1 is expressed in Xenopus oocytes, movement to the cell surface is facilitated by Glycophorin A, although Glycophorin A is not essential for AE1 trafficking (Groves & Tanner, 1992, 1994b). GP.HAG [Gln82 (previously 63) Lys of GPA], GP.MARS [Ala84 (previously 65) Pro of GPA], and GP.ENEV [Val81 (previously 62) Gly of GPA] have an altered expression of Wrb. [citation needed]. OpenUrl . The reactivity of iB5 was further explored by immunostaining following the electrophoretic transfer to nitrocellulose sheets of membrane proteins from common (M and N) and rare erythrocytes [En(a-),S-s-U-, MgMg, McM, St(a+), Mi.V, Mi.III, Tn] … Investig. These include the antigens Mg, Dantu, Henshaw (He), Miltenberger, Nya, Osa, Orriss (Or), Raddon (FR) and Stones (Sta). Jean-pierre Cartron "Molecular genetics of the glycophorin gene family, the antigens for MNSs blood groups: multiple gene rearrangements and modulation of splice site usage result in extensive diversification". 6 (3): 199–209. Michelle P. Lambert, Mortimer Poncz, in Platelets (Third Edition), 2013. and Sta are due to unequal but homologous crossing-over between alpha and delta glycophorin genes. Alloanti-Wrb can be a component in the plasma of immunized En(a–) people. genes are arranged in the same 5' alpha-delta 3' frame whereas Sta gene is in a reciprocal 5'delta-alpha 3' configuration. Stones (Sta) has been shown to be the product of a hybrid gene of which the 5'-half is derived from the glycophorin B whereas the 3'-half is derived from the glycophorin A. This appears to be the origin of one of the Mi-VII specific antigens (Anek) which is known to lie between residues 40-61 of glycophorin A and comprises sialic acid residue(s) attached to O-glycosidically linked oligosaccharide(s). The subclasses were based on additional reactions with other standard antisera. Figure 11.42. GYPA gene consists of 7 exons and has 97% sequence homology with GYPB from the 5' UTR to the coding sequence encoding the first 45 amino acids. Both glycophorin A and B bind the Vicia graminea anti-N lectin. Over 40 antigens have been found in the MNS system. Other investigations have shown that the monoclonal antibody precipitated glycophorin A and B from N+ red cells and only glycophorin B from M+N-erythrocytes. Glycophorin A (GYPA) and B (see 111740), which determine the MN and Ss blood types, respectively, are 2 major receptors that are expressed on erythrocyte surfaces and interact with Plasmodium falciparum ligands. S and s in were described later in 1947. The CD238 molecule is the Kell blood group transmembrane protein [125]. Of these, only MNSs and U are routinely typed. Glycophorin A can rescue the trafficking of some AE1 mutants to the cell surface (see below), including AE1 Southeast Asian ovalocytosis (SAO) (Patterson et al., 2009), certain hereditary spherocytosis (HS) mutants (Toye et al., 2008), and in kAE1, dominant mutations causing distal renal tubular acidosis (dRTA) (Williamson & Toye, 2008; Young et al., 2000). Use for gene localization and for analysis of normal of glycophorin-A-deficient (Finnish type) genomic DNA", "Isolation and characterization of human glycophorin A cDNA clones by a synthetic oligonucleotide approach: nucleotide sequence and mRNA structure", "Molecular cloning of a human glycophorin B cDNA: nucleotide sequence and genomic relationship to glycophorin A. Glycophorin A and B contain MNSs antigens and are well developed at birth. Erythrocyte invasion by malaria (Plasmodium falciparum) merozoites: recent advances in the evaluation of receptor sites. 1986 Sep 25; 261 (27):12433–12436. CD242 is an intercellular adhesion molecule (ICAM4) and represents the Landsteiner–Wiener (LW) blood group antigen(s) [127]. The mature protein SAT protein contains 104 amino acid residues. The very early cells may lack expression of one or more of these markers. As the GPA phenotype in erythrocytes depends on genotypic changes in erythroid precursors, it is impossible to generate in vitro calibration curves. [34], Several viruses bind to glycophorin A including hepatitis A virus (via its capsid),[35] bovine parvovirus,[36] Sendai virus,[37] influenza A and B,[38] group C rotavirus,[39] encephalomyocarditis virus[40] and reoviruses. Emmanuelle Cordat, Reinhart A.F. Some hybrid glycophorin molecules, e.g., Ena.UK, GP.Mur, GP.Hop, GP.Hil, GP.Bun, GP.HF, GP.JL, GP.SAT, GP.TK or GP.Dantu do not express Wrb. Sci. Siebert PD, Fukuda M. Human glycophorin A and B are encoded by separate, single copy genes coordinately regulated by a tumor-promoting phorbol ester. The erythroid precursors are often positive for GPA, hemoglobin A, and CD71 (transferring receptor) (Figure 11.42). Marion E. Reid PhD, FIBMS, DSc (Hon. The myeloblasts in the AML-M6a variant, similar to the myeloblasts in other AMLs, express myeloid-associated markers, such as CD13, CD33, CD117, and MPO, and are often positive for CD34 and HLA-DR. We use cookies to help provide and enhance our service and tailor content and ads. Methods Reagents. AE1 HS mutants that are not rescued by Glycophorin A may have lost the ability to interact with this protein partner due to misfolding. Glycophorins A (GYPA) and B (GYPB) are major sialoglycoproteins of the human erythrocyte membrane which bear the antigenic determinants for the MN and Ss blood groups. [21], Peptide constructs representative of Mia mutations MUT and MUR have been attached onto red blood cells (known as kodecytes) and are able to detect antibodies against these Miltenberger antigens[22][23][24], Although uncommon in Caucasians (0.0098%) and Japanese (0.006%), the frequency of Mi-III is exceptionally high in several Taiwanese aboriginal tribes (up to 90%). These variants include all the variants of the Miltenberger complex and several isoforms of Sta; also, Dantu, Sat, He, Mg, and deletion variants Ena, S-s-U- and Mk. Behring Inst. Glycophorin A (GPA) and glycophorin B (GPB) are the major glycoproteins of the human erythrocyte membrane which carry the MN and the Ss blood group antigens, respec- tively (for reviews see [l, 21). 86, pp. Glycophorin-B. FULL TEXT Abstract: Glycophorins A (GPA) and B (GPB) are two major sialoglycoproteins of the human erythrocyte membrane. This also explains the loss of a high frequency antigen ((EnaKT)) found in normal glycophorin A which is located within the residues 46–56. The time delay before mutated erythroblasts have populated the peripheral blood with mature erythrocytes means that this assay is not suited for the immediate post-accident dosimetry that is required in many situations. Other articles where Glycophorin B is discussed: MNSs blood group system: known as GYPA and GYPB (glycophorin A and B, respectively). A related antigen is Sat. Positive control. The system consists of two pairs of codominant alleles, designated M and N (identified in 1927) and S and s (identified 1947 and 1951, respectively). [18] Mil-IX in contrast is a reverse alpha-delta-alpha hybrid gene. Tanner Mi-I (Mia), Mi-II(Vw), Mi-VII and Mi-VIII are carried on glycophorin A. Mi-I is due to a mutation at amino acid 28 (threonine to methionine: C→T at nucleotide 83) resulting in a loss of the glycosylation at the asparagine26 residue. A new gene closely related to the glycophorin A (GPA) and glycophorin B (GPB) genes has been identified in the normal human genome as well as in that of persons with known alterations of GPA and/or GPB expression. 83, 1665-1669). In individuals who lack both glycophorin A and B the phenotype has been designated Mk. The cross over event which created the genes ancestral to 1984. Flower R, Lin P-H, Heathcote D, Chan M, Teo D, Selkirk A, Shepherd R, Henry S. Insertion of KODE peptide constructs into red cell membranes: Creating artificial variant MNS blood group antigens. [3] GYPA has also recently been designated CD235a (cluster of differentiation 235a). ), ... Martin L. Olsson MD, PhD, in The Blood Group Antigen FactsBook (Third Edition), 2012. 45: Annotation score: Experimental Info. In addition to the M or N and S or s antigens, that commonly occur in all populations, about 40 related variant phenotypes have been identified. The MNS blood group was the second set of antigens discovered. The exon at this point encodes the transmembrane domain.

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