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嘌呤代谢X连锁先天性疾病的分子分析:HPRT1和PRPS1突变

Molecular analysis of X-linked inborn errors of purine metabolism: HPRT1 and PRPS1 mutations.

作者信息

Yamada Yasukazu, Yamada Kenichiro, Nomura Noriko, Yamano Arisa, Kimura Reiko, Naiki Misako, Fukushi Daisuke, Wakamatsu Nobuaki, Taniguchi Atsuo, Yamaoka Noriko, Kaneko Kiyoko, Fujimori Shin

机构信息

Department of Genetics, Institute for Developmental Research, Aichi Human Service Center, Aichi, Japan.

出版信息

Nucleosides Nucleotides Nucleic Acids. 2011 Dec;30(12):1272-5. doi: 10.1080/15257770.2011.597369.

Abstract

Mutations of two enzyme genes, HPRT1 encoding hypoxanthine guanine phosphoribosyltransferase (HPRT) and PRPS1 encoding a catalytic subunit (PRS-I) of phosphoribosylpyrophosphate synthetase, cause X-linked inborn errors of purine metabolism. Analyzing these two genes, we have identified three HPRT1 mutations in Lesch-Nyhan families following our last report. One of them, a new mutation involving the deletion of 4224 bp from intron 4 to intron 5 and the insertion of an unknown 28 bp, has been identified. This mutation resulted in an enzyme polypeptide with six amino acids deleted due to abnormal mRNA skipping exon 5. The other HPRT1 mutations, a single base deletion (548delT, 183fs189X), and a point mutation causing a splicing error (532+1G>A, 163fs165X) were detected first in Japanese patients but have been reported in European families. On the other hand, in the analysis of PRPS1, no mutation was identified in any patient.

摘要

两种酶基因的突变,即编码次黄嘌呤鸟嘌呤磷酸核糖转移酶(HPRT)的HPRT1和编码磷酸核糖焦磷酸合成酶催化亚基(PRS-I)的PRPS1,会导致X连锁嘌呤代谢先天性缺陷。通过对这两个基因的分析,继我们上次报告之后,我们在莱施-奈恩综合征家族中鉴定出了三种HPRT1突变。其中之一是一种新突变,涉及从内含子4到内含子5缺失4224 bp并插入一个未知的28 bp。该突变导致一种酶多肽由于异常的mRNA跳过外显子5而缺失六个氨基酸。另外两种HPRT1突变,一个单碱基缺失(548delT,183fs189X)和一个导致剪接错误的点突变(532+1G>A,163fs165X)首先在日本患者中被检测到,但已在欧洲家族中报道。另一方面,在PRPS1的分析中,未在任何患者中鉴定出突变。

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