Pollak M R, Brown E M, Estep H L, McLaine P N, Kifor O, Park J, Hebert S C, Seidman C E, Seidman J G
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Nat Genet. 1994 Nov;8(3):303-7. doi: 10.1038/ng1194-303.
Defects in the human Ca(2+)-sensing receptor gene have recently been shown to cause familial hypocalciuric hypercalcaemia and neonatal severe hyperparathyroidism. We now demonstrate that a missense mutation (Glu128Ala) in this gene causes familial hypocalcaemia in affected members of one family. Xenopus oocytes expressing the mutant receptor exhibit a larger increase in inositol 1,4,5-triphosphate in response to Ca2+ than oocytes expressing the wild-type receptor. We conclude that this extracellular domain mutation increases the receptor's activity at low Ca2+ concentrations, causing hypocalcaemia in patients heterozygous for such a mutation.
最近研究表明,人类钙离子敏感受体基因缺陷会导致家族性低钙血症性高钙血症和新生儿重症甲状旁腺功能亢进症。我们现在证明,该基因中的一个错义突变(Glu128Ala)导致了一个家族中受影响成员出现家族性低钙血症。表达突变型受体的非洲爪蟾卵母细胞对钙离子的反应比表达野生型受体的卵母细胞产生更大的肌醇1,4,5-三磷酸增加。我们得出结论,这种细胞外结构域突变在低钙离子浓度下增加了受体的活性,导致杂合这种突变的患者出现低钙血症。