Quantitative Analysis of Lea and Le^b Antigens in Human Saliva

Wang, Baojie; Akiyama, Kanji; Kimura, Hiroshi

doi:10.1159/000462531

Cited by 6 publications

(7 citation statements)

References 24 publications

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“…The Lewis antigens are not intrinsic to red blood cells but are absorbed onto red blood cell membranes from the plasma. Accordingly, typing of Lewis phenotypes is difficult and is sometimes misjudged because of weak hemagglutination as a result of the small numbers of the antigens on red cells, and low titers and low specificities of anti-Le a and anti-Le b antibodies (Good et al 1992;Wang et al 1994). Therefore, it is important and useful to determine the genotypes of the Lewis system.…”

Section: Hao Pang · Yuhua Liu · Yoshiro Koda · Mikiko Soejima Jingtaomentioning

confidence: 99%

Five novel missense mutations of the Lewis gene (FUT3) in African (Xhosa) and Caucasian populations in South Africa

Pang¹,

Liu²,

Koda³

et al. 1998

Hum Genet

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Five novel missense mutations, viz., C304 A, T370 G, G484 A, G667 A, and G808 A, in the Lewis gene (FUT3) were detected in African (Xhosa) and Caucasian individuals in South Africa. These single base substitutions may result in changes in amino acid residues from Gln102 to Lys in the 304 mutation, Ser124 to Ala in the 370 mutation, Asp162 to Asn in the 484 mutation, Gly223 to Arg in the 667 mutation, and Val270 to Met in the 808 mutation. Out of the five novel mutations identified in this investigation, four new alleles (le484,667, le484,667,808, Le304, and Le370) were determined in the Xhosa population and two new alleles (le202,314,484 and Le304) in the Caucasian population. The determination of alpha(1,3/1,4)fucosyltransferase activity, after transfection of plasmids containing the new alleles into COS7 cells, suggested that alleles le484,667 and le484,667,808 encoded an inactive enzyme, and that alleles Le304 and Le370 encoded a functional enzyme. In addition, we also examined the incidence of five common alleles, Le59, le59,508 le59,1067, le202,314, and le1067 in two populations by the polymerase chain reaction/restriction fragment length polymorphism method and compared differences in the allele frequencies of FUT3 among three ethnic groups (Orientals, Africans, and Caucasians).

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Section: Hao Pang · Yuhua Liu · Yoshiro Koda · Mikiko Soejima Jingtaomentioning

confidence: 99%

Five novel missense mutations of the Lewis gene (FUT3) in African (Xhosa) and Caucasian populations in South Africa

Pang¹,

Liu²,

Koda³

et al. 1998

Hum Genet

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“…The blood group and saliva secretion tests of a para-Bombay individual were performed as described previously [11]. A further 136 randomly selected blood samples were provided by the Japan Red Cross Blood Center in Fukuoka City, and genomic DNA was isolated from peripheral leukocytes by the standard method [12].…”

Section: Blood Typingmentioning

confidence: 99%

Two Missense Mutations of H Type α(1,2)Fucosyltransferase Gene (FUT1) Responsible for Para-Bombay Phenotype

et al. 1997

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Background and objectives: Rare individuals (Bombay and para-Bombay phenotypes) fail to express the A, B and H antigens on erythrocyte membranes because of a lack in the //gene (FUT1)-encoded α(l,2)fucosyltransferase activity. In this study, we have found a para-Bombay individual (B(m)^h) who expressed B and H antigens in saliva but not on red blood cells. The FUT1 alleles of this person contained two single base changes (T460C and G1042A) in the coding region relative to the wild type allele. These substitutions may result in changes in two amino acid residues (Y154H and E348K). Materials and methods: Since the T460C and G1042A mutations destroy endonuclease RsaI and AvaI sites, respectively, we tested for these mutations using PCR-RFLP. Results: Our findings indicated that this para-Bombay person was homozygous for the T460C and G1042A mutations, and that neither of these mutations was found in 136 randomly selected Japanese individuals. The measurement of the α(l,2)fucosyltransferase activity after transient expression of the FUTI alleles in COS-7 cells indicated that the H-deficient allele-encoded enzyme had no detectable activity. Moreover, transfection by chimera FUT1 allele contains only the T460C mutation, or only the G1042A mutation, and yielded 1.0 or 9.3%, respectively, of the activities compared to transfection by the wild type allele. Conclusions: These results suggest that the two mutations in combination are responsible for the inactivation of the FUT1-encoded enzyme activity.

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“…The a(l,2)fucosyltransferase that forms the H antigen, an essential precursor of the A and B antigens, plays a regulatory role in the tissue expression of the ABO antigens. Several lines of evidence have indicated that at least two a( 1,2)fucosyltransferases are present in human tissues [6, 71. One is the H-type FUTl-encoded a(l,2)fucosyltransferase, which regulates the expression of the H antigen mainly on erythrocyte membranes and the other is the secretortype FUT2-encoded a( 1,2)fucosyltransferase, which regulates the expression of the H antigen mainly in epithelial cells and body fluids such as saliva [4,5,[8][9][10]. FUTI, FUT2, and a FUT2 pseudogene (Secl) have been isolated [ll-131.…”

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confidence: 99%

Structure and Expression of the Gene Encoding Secretor‐Type Galactoside 2‐α‐l‐fucosyltransferase (FUT2)

Koda

Soejima

Wang

et al. 1997

European Journal of Biochemistry

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The expression and secretion of ABO antigens in epithelial cells of glands are controlled by secretortype a(l,2)fucosyltransferase activity. We have examined the expression of the secretor-type a( 1,2)fucosyltransferase gene (FUT2) and a pseudogene of FUT2 (Secl) in several tumor cell lines by northern blot and/or reverse-transcription-PCR (RT-PCR) analyses. Transcripts of FUT2 were found in total RNA from ovarian, gastric and colonic cancer cell lines but not from six leukemic cell lines, including erythroleukemic HEL cells, by RT-PCR. On the other hand, RT-PCR indicated that Secl was expressed in all these tumor cells, including all hematopoietic cells studied. Northern blot analysis indicated that FUT2 transcripts with a similar size (3.3 kb) were expressed in cancer cell lines. Rapid amplification of cDNA ends suggested that the entire FUT2 cDNA is 3.1-kb long and has two Alu repetitive elements in its 3' untranslated region, including an inverted repeat. The mRNA, therefore, may form a large stem-and-loop structure (1.2 kb). Each stem contains about 300 bases, the loop contains 640 bases, and the percentage of complementary nucleotide sequences in the stem region is 85%. The presence of a large stem-andloop structure in the 3' untranslated region may regulate the level of the FUT2 transcript by affecting the stability of the mRNA.

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Quantitative Analysis of Lea and Le^b Antigens in Human Saliva

Cited by 6 publications

References 24 publications

Five novel missense mutations of the Lewis gene (FUT3) in African (Xhosa) and Caucasian populations in South Africa

Five novel missense mutations of the Lewis gene (FUT3) in African (Xhosa) and Caucasian populations in South Africa

Two Missense Mutations of H Type α(1,2)Fucosyltransferase Gene (FUT1) Responsible for Para-Bombay Phenotype

Structure and Expression of the Gene Encoding Secretor‐Type Galactoside 2‐α‐l‐fucosyltransferase (FUT2)

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