Hansen J L, Pryor M A, Kennedy J B, Kushner J P
Division of Hematology/Oncology, University of Utah Medical Center, Salt Lake City 84132.
Am J Hum Genet. 1988 Jun;42(6):847-53.
Familial porphyria cutanea tarda (PCT) results from a generalized deficiency of uroporphyrinogen decarboxylase (URO-D) activity. The molecular defect responsible for this disorder has not been characterized. To determine whether decreased levels of URO-D mRNA are responsible for subnormal URO-D activity, steady-state levels of URO-D mRNA in lymphoblastoid cells were determined. Northern blots were hybridized with a URO-D cDNA probe and quantified by densitometry. No difference in the levels of URO-D mRNA was detected between affected individuals and their normal relatives. Thus, the deficiency of URO-D activity in two familial PCT pedigrees characterized here does not arise from a deficiency of URO-D mRNA.
家族性迟发性皮肤卟啉症(PCT)是由尿卟啉原脱羧酶(URO-D)活性普遍缺乏引起的。导致这种疾病的分子缺陷尚未明确。为了确定URO-D mRNA水平降低是否是URO-D活性低于正常水平的原因,我们测定了淋巴母细胞中URO-D mRNA的稳态水平。Northern印迹用URO-D cDNA探针杂交,并通过光密度测定法进行定量。在受影响个体及其正常亲属之间未检测到URO-D mRNA水平的差异。因此,这里所描述的两个家族性PCT家系中URO-D活性的缺乏并非源于URO-D mRNA的缺乏。