Basis of unique red cell membrane properties in hereditary ovalocytosis

Schofield, Ann E.; Tanner, Michael; Pinder, Jennifer C.; Clough, Barbara; Bayley, Peter M.; Nash, Gerard B.; Dluzewski, Anton R.; Reardon, David M.; Cox, Timothy M.; Wilson, Robert; Gratzer, Walter

doi:10.1016/0022-2836(92)90254-h

Cited by 96 publications

(52 citation statements)

References 48 publications

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“…Because genetic mutations can provide resistance to malarial infection, malarial selection is suggested to determine the frequency of genetic disease in human population (Flint et aL, 1993). Our results confirmed that ovalocytosis in an isolated Indonesian island presents with the same amino acid deletion of the band 3 protein as reported in other countries (Tanner et al, 1991;Mohandas et al, 1992;Schofield et al, 1992;Takeshima et aL, 1994). This is the second example of a genetic disease that is common in endemic malarious regions and is caused by only one kind of mutation, If it is true that only one mutation is common in areas from Melanesia to Mauritius, what factor may provide such phenomenon?…”

Section: Bp 148 Bpsupporting

confidence: 85%

Deletion of twenty seven nucleotides within exon 11 of the band 3 gene identified in ovalocytosis in Lombok Island, Indonesia

et al. 1997

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SummaryThis study reports the molecular characterization of ovalocytosis in Lombok Island, Indonesia. The analysis of genomic DNA by polymerase chain reaction shows that all 2I ovalocytotic individuals have two amplified products of different size from a region encompassing exon 11 of the band 3 gene. The sequence of the larger product matched perfectly with that of normal individuals. In the sequence of the smaller product, 27 nucleotides within exon 11 were deleted. The heterozygous presence of the deletion identified in other parts of Southeast Asia was confirmed in patients with ovalocytosis in an isolated island of eastern Indonesia.

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Section: Bp 148 Bpsupporting

confidence: 85%

Deletion of twenty seven nucleotides within exon 11 of the band 3 gene identified in ovalocytosis in Lombok Island, Indonesia

et al. 1997

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“…19 Synthetic peptides based on these sequences inhibited adherence of infected erythrocytes to melanoma cells in vitro and appeared to prevent sequestration when infused into P. falciparum-infected Aotus and Saimiri monkeys. 20 The deletion of amino acids 400-408 in SAO band 3 markedly increases the rigidity of the red blood cell membrane 21 and may prevent the expression of the cytoadherent sequences. Also, in view of the reduced expression of several blood group antigens 22 in ovalocytic red blood cells, the expression of other red blood cell cytoadherence ligands might also be reduced.…”

Section: Discussionmentioning

confidence: 99%

Prevention of cerebral malaria in children in Papua New Guinea by southeast Asian ovalocytosis band 3.

Allen¹,

O’Donnell²,

Nast³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

156

116

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Abstract. Southeast Asian ovalocytosis (SAO) occurs at high frequency in malarious regions of the western Pacific and may afford a survival advantage against malaria. It is caused by a deletion of the erythrocyte membrane band 3 gene and the band 3 protein mediates the cytoadherence of parasitized erythrocytes in vitro. The SAO band 3 variant may prevent cerebral malaria but it exacerbates malaria anemia and may also increase acidosis, a major determinant of mortality in malaria. We undertook a case-control study of children admitted to hospital in a malarious region of Papua New Guinea. The SAO band 3, detected by the polymerase chain reaction, was present in 0 of 68 children with cerebral malaria compared with six (8.8%) of 68 matched community controls (odds ratio ϭ 0, 95% confidence interval ϭ 0-0.85). Median hemoglobin levels were 1.2 g/dl lower in malaria cases with SAO than in controls (P ϭ 0.035) but acidosis was not affected. The remarkable protection that SAO band 3 affords against cerebral malaria may offer a valuable approach to a better understanding of the mechanisms of adherence of parasitized erythrocytes to vascular endothelium, and thus of the pathogenesis of cerebral malaria.

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“…9 The cause of SAO is a heterozygous presence of a deletion of amino acids 400 to 408, inclusive, at the cytoplasmic boundary in the first membrane span of band 3 (B3SAO). 10 The abnormal protein does not mediate chloride transport, 11 and homozygosity for B3SAO appears to be lethal. 12 SAO erythrocytes have been reported to show a selective depression of several RBC antigens.…”

Section: Introductionmentioning

confidence: 99%

Coexpression of band 3 mutants and Rh polypeptides: differential effects of band 3 on the expression of the Rh complex containing D polypeptide and the Rh complex containing CcEe polypeptide

Beckmann

Smythe

Anstee

et al. 2001

Blood

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Basis of unique red cell membrane properties in hereditary ovalocytosis

Cited by 96 publications

References 48 publications

Deletion of twenty seven nucleotides within exon 11 of the band 3 gene identified in ovalocytosis in Lombok Island, Indonesia

Deletion of twenty seven nucleotides within exon 11 of the band 3 gene identified in ovalocytosis in Lombok Island, Indonesia

Prevention of cerebral malaria in children in Papua New Guinea by southeast Asian ovalocytosis band 3.

Coexpression of band 3 mutants and Rh polypeptides: differential effects of band 3 on the expression of the Rh complex containing D polypeptide and the Rh complex containing CcEe polypeptide

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