Thomas P M, Cote G J, Wohllk N, Haddad B, Mathew P M, Rabl W, Aguilar-Bryan L, Gagel R F, Bryan J
Department of Medical Specialties, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
Science. 1995 Apr 21;268(5209):426-9. doi: 10.1126/science.7716548.
Familial persistent hyperinsulinemic hypoglycemia of infancy (PHHI), an autosomal recessive disorder characterized by unregulated insulin secretion, is linked to chromosome 11p14-15.1. The newly cloned high-affinity sulfonylurea receptor (SUR) gene, a regulator of insulin secretion, was mapped to 11p15.1 by means of fluorescence in situ hybridization. Two separate SUR gene splice site mutations, which segregated with disease phenotype, were identified in affected individuals from nine different families. Both mutations resulted in aberrant processing of the RNA sequence and disruption of the putative second nucleotide binding domain of the SUR protein. Abnormal insulin secretion in PHHI appears to be caused by mutations in the SUR gene.
家族性婴儿持续性高胰岛素血症性低血糖症(PHHI)是一种常染色体隐性疾病,其特征为胰岛素分泌失调,与11号染色体p14 - 15.1区域相关。新克隆的高亲和力磺脲类受体(SUR)基因是胰岛素分泌的调节因子,通过荧光原位杂交将其定位于11p15.1。在来自九个不同家族的患病个体中鉴定出两个与疾病表型分离的独立SUR基因剪接位点突变。这两种突变均导致RNA序列加工异常,并破坏了SUR蛋白假定的第二个核苷酸结合结构域。PHHI中异常的胰岛素分泌似乎是由SUR基因突变引起的。