Ludwig M, Schwaab R, Eigel A, Horst J, Egli H, Brackmann H H, Olek K
Institute of Experimental Haematology and Blood Transfusion, Bonn, Federal Republic of Germany.
Am J Hum Genet. 1989 Jul;45(1):115-22.
DNA of 70 unrelated hemophilia B patients, including three inhibitor patients, was analyzed by using various restriction enzymes and was hybridized with both a factor IX cDNA and 3'- and 5'-flanking probes. When the gene was mapped this way, six patients all afflicted with severe hemophilia B were shown to have a deviating hybridization pattern. One inhibitor patient showed a partial deletion of about 9 kb that removes exons a-c. A partial deletion of at least 11 kb that removed exon a and that had a maximum size of 35 kb in the 5'-flanking region could be identified in a patient of unknown status. In another three noninhibitor patients a complete deletion of the factor IX gene and two partial deletions could be observed. The partial deletions are of approximately 8 kb and approximately 1.5 kb, removing exons d and e and exon g, respectively. As detected by oligonucleotide probing, a C-to-T transition at amino acid 338 gave rise to an altered TaqI restriction pattern that could be observed in a sixth patient. The other 64 hemophilia B patients, including two inhibitor patients, showed a hybridization pattern indistinguishable from a normal one.
对70名无亲缘关系的B型血友病患者(包括3名产生抑制剂的患者)的DNA进行分析,使用了多种限制性内切酶,并使其与因子IX cDNA以及3'和5'侧翼探针杂交。当以这种方式对基因进行定位时,发现6名均患有严重B型血友病的患者呈现出异常的杂交模式。1名产生抑制剂的患者显示约9 kb的部分缺失,该缺失去除了外显子a - c。在1名情况不明的患者中,可鉴定出至少11 kb的部分缺失,该缺失去除了外显子a,且在5'侧翼区域最大为35 kb。在另外3名非产生抑制剂的患者中,可观察到因子IX基因的完全缺失和两个部分缺失。部分缺失分别约为8 kb和约1.5 kb,分别去除了外显子d和e以及外显子g。通过寡核苷酸探针检测,第6名患者中氨基酸338处的C到T转换导致TaqI限制性模式改变。其他64名B型血友病患者(包括2名产生抑制剂的患者)显示出与正常模式无法区分的杂交模式。