Disease relevance of GYPA

• Association of blood groups with essential and secondary hypertension. A possible association of the MNS system [1].
• To determine which polyadenylation signals are utilized, cDNA clones encoding GPA were isolated from a cDNA library of human erythroleukemia cell line K562 and the 3'-regions of the cDNAs were specifically amplified by the polymerase chain reaction [2].
• The minor, although highly significant, changes which were recognized in the PAS pattern of beta-thalassemia patients compared with normal controls concerned the PAS-4 region and a shoulder trailing band PAS-2, which both increased in staining intensity relatively to the main sialocomponent PAS-1 [3].
• The isolated vesicles maintain their cytoplasmic integrity and normal membrane orientation, and are resistant to hemolysis over the pH range 5.0 - 11.0 and temperature range 4-50 degrees C. The only membrane proteins detected in vesicles from human erythrocytes were band 3 region polypeptides and bands PAS-1, PAS-2 and PAS-3 [4].
• Tn and MN glycoproteins were equally potent inhibitors of influenza virus HA [5].

Psychiatry related information on GYPA

• The best predictors for GPA were academic self-efficacy and achievement motivation (ps =.496 and.303, respectively) [6].
• Serial samples from 40 heavy smokers ( > or = pack/day for > or = 1 year) enrolled in a smoking cessation program were assayed for cotinine, polycyclic aromatic hydrocarbon (PAH)-DNA, 4-aminobiphenyl-hemoglobin (4-ABP-Hb) adducts, and glycophorin A (GPA) mutations [7].
• Depression, self-esteem, suicide ideation, death anxiety, and GPA in high school students of divorced and nondivorced parents [8].
• Negative correlations among scores on competitiveness, GPA, and scores on internal locus of control were significant [9].
• An ethnically diverse group of college students reported their GPA and responded to the Parenting Style Index [10].

High impact information on GYPA

• Using antibodies directed against different structural regions of the major sialoglycoprotein alpha, we confirm here and two variant erythrocytes (Miltenberger class V (MiV) and Ph) contain hybrid sialoglycoprotein molecules (Fig. 1). These hybrid sialoglycoproteins arise from cross-over events between the genes coding for alpha and delta [11].
• The spontaneous and induced VFs agree with previous measurements of radiation-induced mutagenesis in other systems; this evidence supports a mutational origin for variant cells characterized by a loss of GPA expression and suggests that the GPA assay system may provide a cumulative dosimeter of past radiation exposures [12].
• Like the early blood-group markers (e.g., Rh and MNS), tightly linked biallelic SNPs can be combined into composite markers with heterozygosity similar to that of short-tandem-repeat polymorphisms [13].
• Thus, these results suggest that benzene produces gene-duplicating mutations but does not produce gene-inactivating mutations at the GPA locus in bone marrow cells of humans exposed to high benzene levels [14].
• NN variants result from loss of the GPA M allele and duplication of the N allele, presumably through recombination mechanisms, whereas NO variants arise from gene inactivation, presumably due to point mutations and deletions [14].

Chemical compound and disease context of GYPA

• Deposition of PAS2-positive materials and thickening of the basement membrane in vascular lesions are characteristic findings in diabetes mellitus, suggesting altered metabolism of glycoprotein [15].

Biological context of GYPA

• CONCLUSIONS: The GP.Hop phenotype is produced by a hybrid GP(B-A-B) protein caused by a DNA insertion of GYPA into GYPB [16].
• PCR-amplified products of the coding exons of GYPA were studied by single-strand conformation polymorphism analysis, and exon 3 was sequenced [17].
• Those restriction fragments characteristic of the GPA 3' and GPB 5' ends were absent from the SAT homozygote and showed reduced intensity in SAT heterozygotes [18].
• The low-frequency MNS blood group antigens Ny(a) (MNS18) and Os(a) (MNS38) are associated with GPA amino acid substitutions [17].
• These results provide further insight into the model for evolution of the GPA gene family, indicating that the mechanisms underlying inter- and intraspecific polymorphism of glycophorins could predate the divergence of gorillas as the consequence of gene duplication and diversification [19].

Anatomical context of GYPA

• There are 3-4 times more copies of GPA as compared with GPB on human erythrocytes (10(6) versus 2 x 10(5) copies/cell), whereas GPE is absent or poorly represented [20].
• Analysis of chimerism in immature (glycophorin A-positive [GYPA(+)], CD71(hi)) and mature (GYPA(+), CD71(neg)) erythroblasts confirmed the intramedullary loss of SS erythroblasts with progressive maturation [21].
• Human red cell glycophorin A (GPA) enhances the expression of band 3 anion transport activity at the cell surface of Xenopus oocytes [22].
• GPA may affect the rate of accumulation of band 3 at the cell surface, rather than the final level in the plasma membrane [23].
• Other GPA-independent mechanisms must also allow translocation of band 3 to the surface membrane in erythroid cells and oocytes [23].

Associations of GYPA with chemical compounds

• The coexpression of GPA with band 3 increased stilbene disulfonate-sensitive chloride transport into the oocytes [23].
• The present study also revealed that this Sta individual has a variant GPA gene; substitution of adenine for guanine at the nucleotide for codon 39 results in substitution of lysine for arginine at amino acid 39, and loss of an SstI restriction site [24].
• The GPA-deficient cells had a normal K(d) for iodide binding, in agreement with the unchanged K(m) found in transport studies [25].
• The co-expression of GPA with either glycosylated or unglycosylated b3 increased the stilbene disulphonate-sensitive chloride transport into oocytes at low cRNA concentrations [26].
• V glycoprotein (donor F. M.) contains approximately 60 amino acid residues of GPA at its N-terminus [27].

Physical interactions of GYPA

• The sialoglycoprotein PAS 2 has also been shown to interact with cytoskeleton and has been named glycoconnectin [28].

Regulatory relationships of GYPA

• Glycophorins A (GPA) and B (GPB) are specifically expressed in human erythrocytes and express MN and Ss blood group antigens [2].

Other interactions of GYPA

• GPA transcripts were very stable (at least 24 h), whereas GPB transcripts were severely reduced after 17 h [20].
• STUDY DESIGN AND METHODS: Taking advantage of the differences between the GPA and GPB genes, a polymerase chain reaction-based method was developed to detect all the Miltenberger glycophorin variants and St(a) subtype [29].
• BACKGROUND: The GP.Hop (Mi.IV) phenotype expresses the MNS low-incidence antigens Mur, Hop, TSEN, MINY, and MUT [16].
• Population data were generated for the loci LDLR, GYPA, HBGG, D7S8, Gc, HLA-DQA1, and D1S80 from 180 Arabs from Dubai [30].
• The dendrograms based on six coding loci (HLDQA1, LDLR, GYPA, HBGG, D7S8, GC) differs from those based on STR and VNTR markers [31].

Analytical, diagnostic and therapeutic context of GYPA

• MATERIALS AND METHODS: Following RT-PCR amplification of total RNA isolated from one Vr+ person (G488) and one Mt(a+) person (GH), the genes encoding glycophorin A (GYPA) and glycophorin B (GYPB) were cloned and sequenced [32].
• Immunoblotting with anti-Os(a) and an MAIEA assay with MoAbs to GPA showed that Os(a) is on GPA [17].
• Distribution of alleles of three tetrameric STR loci HUMHPRTB, HUMF13B, HUMLPL and other six PCR based loci HLA DQA1, LDLR, GYPA, HBGG, D7S8, Gc in eight predominant populations of India [33].
• Japanese population DNA typing data for the loci LDLR, GYPA, HBGG, D7S8, and GC [34].
• The effects of blood transfusions on PCR DNA typing at the CSF1P0, TP0X, TH01, D1S80, HLA-DQA1, LDLR, GYPA, HBGG, D7S8 and GC loci [35].

References