Aalto-Setälä K
Recombinant DNA Laboratory, University of Helsinki, Finland.
FEBS Lett. 1988 Jul 18;234(2):411-6. doi: 10.1016/0014-5793(88)80127-3.
In one third of Finnish patients with the heterozygous form of familial hypercholesterolemia the disease is due to a gross deletion at the 3'-end of the LDL receptor gene. The present study demonstrates that an 8-kb deletion completely eliminates exons 16 and 17 and a part of exon 18. Cloning and partial sequencing of a DNA fragment from the mutated allele indicated that the 5'-boundary of the deletion lies within intron 15 while the 3'-breakpoint is located at nucleotide 3390 in exon 18. RNA blot hybridization studies revealed that the mutated allele encodes a truncated 4.2 kb mRNA (normal, 5.3 kb). This type of mutation has not been reported in other ethnic groups.
在三分之一的芬兰杂合型家族性高胆固醇血症患者中,该病是由于低密度脂蛋白受体基因3'端的大片段缺失所致。本研究表明,一个8 kb的缺失完全消除了外显子16和17以及外显子18的一部分。对来自突变等位基因的DNA片段进行克隆和部分测序表明,缺失的5'边界位于内含子15内,而3'断点位于外显子18的第3390个核苷酸处。RNA印迹杂交研究显示,突变等位基因编码一个截短的4.2 kb mRNA(正常为5.3 kb)。这种类型的突变在其他种族群体中尚未见报道。