Shuto Y, Wakabayashi I, Amuro N, Minami S, Okazaki T
Department of Medicine, Nippon Medical School, Tokyo, Japan.
J Clin Endocrinol Metab. 1992 Jul;75(1):213-7. doi: 10.1210/jcem.75.1.1619012.
A tight linkage between generalized resistance to thyroid hormone (GRTH) and the thyroid hormone receptor-beta (TR beta) gene is indicated. We evaluated a family with GRTH for the TR beta gene. We found that a new point mutation, consisting of a cytosine to adenine replacement at nucleotide position 1642, resulted in substitution in codon 448 in the T3-binding domain of TR beta. This base substitution was found in only one allele of affected members, but not in unaffected members of the family. The in vitro translation products of this mutant TR beta gene demonstrated significantly reduced T3-binding affinity. Previously, others have reported a kindred with GRTH, in that the same codon was subjected to proline to histidine replacement due to a mutation consisting of a cytosine to adenine replacement at nucleotide position 1643. There appeared to be a significant phenotypic difference between our kindred and that described by others.
结果表明,全身性甲状腺激素抵抗(GRTH)与甲状腺激素受体β(TRβ)基因之间存在紧密联系。我们对一个患有GRTH的家系进行了TRβ基因评估。我们发现一个新的点突变,即在核苷酸位置1642处胞嘧啶被腺嘌呤取代,导致TRβ的T3结合结构域中第448密码子发生替换。这种碱基替换仅在患病成员的一个等位基因中发现,而在该家系的未患病成员中未发现。该突变TRβ基因的体外翻译产物显示T3结合亲和力显著降低。此前,其他人曾报道过一个患有GRTH的家族,由于在核苷酸位置1643处胞嘧啶被腺嘌呤取代的突变,同一密码子发生了脯氨酸被组氨酸替换的情况。我们的家族与其他人描述的家族之间似乎存在显著的表型差异。