Suppr超能文献

[磷酸核糖焦磷酸合成酶活性增加]

[Increased activity of PRPP synthetase].

作者信息

Iizasa Taizo

机构信息

Department of Internal Medicine, Itoh Municipal Hospital.

出版信息

Nihon Rinsho. 2008 Apr;66(4):694-8.

Abstract

PRPP(phosphoribosyl pyrophosphate) synthetase catalyzes the formation of PRPP from ATP and ribose 5-phosphate. Human PRPP synthetase exists as heterogeneous aggregates composed of the 34kDa catalytic subunits (PRSI and PRSII) and other 39kDa and 41kDa components designated PRPP synthetase-associated protein (PAP39 and PAP41). A syndrome of increased activity of PRPP synthetase, an X-linked dominant-inherited disorder, is one of the models of gout caused by increased production of uric acid. By now, around twenty cases have been reported over the world. Two different molecular mechanisms underlie this syndrome: (1) point mutation in the gene coding the primary structure of PRPP synthetase causes the substitution of an amino acid residue and, consequently, the regulatory defects, those are resistant traits to allosteric nucleotide feedback inhibition; (2) increased transcription of PRPP synthetase mRNA causes overproduction of this enzyme protein. The mechanism producing increased mRNA is, however, not elucidated. The Japanese case has been found to be caused by the second mechanism.

摘要

磷酸核糖焦磷酸(PRPP)合成酶催化由ATP和5-磷酸核糖形成PRPP。人PRPP合成酶以异源聚集体形式存在,由34kDa催化亚基(PRSI和PRSII)以及其他39kDa和41kDa组分组成,这些组分被称为PRPP合成酶相关蛋白(PAP39和PAP41)。PRPP合成酶活性增加综合征是一种X连锁显性遗传性疾病,是尿酸生成增加导致痛风的模型之一。到目前为止,全世界已报道了约20例病例。该综合征有两种不同的分子机制:(1)编码PRPP合成酶一级结构的基因中的点突变导致氨基酸残基的替换,从而导致调节缺陷,这些是对变构核苷酸反馈抑制的抗性特征;(2)PRPP合成酶mRNA转录增加导致该酶蛋白过量产生。然而,导致mRNA增加的机制尚未阐明。已发现日本的病例是由第二种机制引起的。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验