Molecular basis for H blood group deficiency in Bombay (Oh) and para-Bombay individuals.

Kelly, Robert J.; Эрнст, Л. К.; Larsen, Robert D.; Bryant, Jane G.; Robinson, Judy S.; Lowe, John B.

doi:10.1073/pnas.91.13.5843

Cited by 169 publications

(125 citation statements)

References 18 publications

(17 reference statements)

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“…2 C). A 5′-RACE product of about 350 bp was amplified from ECV304 cells (data not shown) and the results of DNA sequence analysis indicated that the 5′ ends of 10 clones of the RACE products from ECV304 cells were present between 1 bp and 27 bp downstream of the transcription start site of the FUT1 previously reported in A431 cells [17]. In addition, primer-extension analysis supported that the transcription start site of the FUT1 in ECV304 cells was possibly identical to that in A431 cells (data not shown).…”

Section: Resultsmentioning

confidence: 93%

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Changing transcription start sites in H‐type α(1,2)fucosyltransferase Gene (FUT1) during differentiation of the human erythroid lineage

Koda

Soejima

Kimurâ

1998

European Journal of Biochemistry

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Recent studies have suggested that at least three transcription-initiation sites were present in the human H-type A(1,2)fucosyltransferase gene (FUT1). In the present study, we have investigated these transcription start sites of FUT1 in undifferentiated leukemic cells (K562) that have erythroid characteristics, in erythroleukemia cells (HEL), and in bone marrow cells. K562 cells used exclusively exon 1 as the start site. While HEL cells used mainly exon 2 as the start site, the major start site for bone marrow cells was within exon 7. In addition, we investigated the transcription start site(s) in vascular endothelial cells (ECV304) as an example of mature cells and found that the start site was predominantly within exon 7. The promoter activities were found in the 5′ flanking regions of these three start sites after transfection of constructs with luciferase reporter gene into K562 and HEL cells. These findings suggested that the transcription start sites of FUT1 changed during differentiation of the erythroid lineage and that the tissue-specific and stage-specific expressions of the FUT1 were regulated by three distinct promoters. We also found that the 5′ flanking region of exon 2 (intron 1) consisted of repetitive sequences (chromosome 19-specific 37-bp minisatellite repeats, Alu sequence and long terminal repeat) and that the start site of exon 2 was within the long terminal repeat. Thus, these repetitive sequences may play a role in the expression of the FUT1.

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Section: Resultsmentioning

confidence: 93%

“…Recently, Kelly et al [17] reported a transcription initiation site of FUT1 in A431 cells. In addition, we have reported the gene structure of the FUT1 and two new transcription initiation sites, different from that in the A431 cells, in human bone marrow and some cancer cells including MCAS (ovarian cancer) cells [18].…”

mentioning

confidence: 99%

Changing transcription start sites in H‐type α(1,2)fucosyltransferase Gene (FUT1) during differentiation of the human erythroid lineage

Koda

Soejima

Kimurâ

1998

European Journal of Biochemistry

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“…The H and secretor blood group loci determine the expression of these enzymes, which construct Fuc ␣162Gal␤-linkages (H determinants) that are essential precursors to the A and B Ags. Erythrocytes from rare Bombay blood group phenotype individuals are deficient in H determinants, and consequently A and B, the likely result of homozygosity for null alleles at the H locus (32). To date, Bombay individuals have never been examined specifically for angiogenic deficits, probably because no biologic relevance of the H Ag has been determined (33).…”

Section: Lementioning

confidence: 99%

“…One of the final steps in the biosynthesis of ABO blood group oligosaccharide Ags in vivo is catalyzed by ␣-(1,2)-fucosyltransferase(s) (32). The H and secretor blood group loci determine the expression of these enzymes, which construct Fuc ␣162Gal␤-linkages (H determinants) that are essential precursors to the A and B Ags.…”

Section: Lementioning

confidence: 99%

Ley/H: An Endothelial-Selective, Cytokine-Inducible, Angiogenic Mediator

Halloran

Carley

Polverini

et al. 2000

The Journal of Immunology

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Endothelial cells (ECs) are key participants in angiogenic processes that characterize tumor growth, wound repair, and inflammatory diseases, such as human rheumatoid arthritis (RA). We and others have shown that EC molecules, such as soluble E-selectin, mediate angiogenesis. Here we describe an EC molecule, Lewisy-6/H-5-2 glycoconjugate (Ley/H), that shares some structural features with the soluble E-selectin ligand, sialyl Lewisx (sialyl Lex). One of the main previously recognized functions of Lewisy is as a blood group glycoconjugate. Here we show that Ley/H is rapidly cytokine inducible, up-regulated in RA synovial tissue, where it is cell-bound, and up-regulated in the soluble form in angiogenic RA compared with nonangiogenic osteoarthritic joint fluid. Soluble Ley/H also has a novel function, for it is a potent angiogenic mediator in both in vitro and in vivo bioassays. These results suggest a novel paradigm of soluble blood group Ags as mediators of angiogenic responses and suggest new targets for therapy of diseases, such as RA, that are characterized by persistent neovascularization.

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“…This results in what is referred to as the Bombay phenotype (Oh) [1][2][3][4][5][6][7][8][9][10][11][12][13] . In Bombay blood group individuals there is anti-A, anti-B, anti-AB and anti-H which are all active at 37 0 C 2-5 , [11][12][13][14][15][16] .The use of Anti-H lectin and detection of secretor status by using saliva are also important for diagnosis, as the Bombay group people are non secretors 4,5 . In Bangladesh at present ABO and Rh typing is done by forward grouping in the vast majority of cases.…”

Section: Discussionmentioning

confidence: 99%

Bombay Phenotype: Report of 2 Cases

Dipta

Hossain

Khatun

et al. 2012

J. Bangladesh Coll. Phys.

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Summary:Two cases of the rare blood group "Bombay phenotype" are discussed here. This rare blood group, Bombay (Oh) was first established by Bhende et al in Bombay (Mumbai), in 1952.In the ABO (ABH) blood group system, the 'O' antigen represents the lack of A or B antigens; however it has the most amount of H antigen. If the H gene is absent, which is extremely rare, H substance can not be formed and subsequent A and B antigens can not also be formed. Absence of H gene results in the Bombay phenotype (Oh) 1-6, 7-13 .

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Molecular basis for H blood group deficiency in Bombay (Oh) and para-Bombay individuals.

Cited by 169 publications

References 18 publications

Changing transcription start sites in H‐type α(1,2)fucosyltransferase Gene (FUT1) during differentiation of the human erythroid lineage

Changing transcription start sites in H‐type α(1,2)fucosyltransferase Gene (FUT1) during differentiation of the human erythroid lineage

Ley/H: An Endothelial-Selective, Cytokine-Inducible, Angiogenic Mediator

Bombay Phenotype: Report of 2 Cases

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