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1
Sequencing of Aspergillus nidulans and comparative analysis with A. fumigatus and A. oryzae.构巢曲霉的测序以及与烟曲霉和米曲霉的比较分析。
Nature. 2005 Dec 22;438(7071):1105-15. doi: 10.1038/nature04341.
2
4-Hydroxyphenylpyruvate dioxygenase.4-羟基苯丙酮酸双加氧酶
Arch Biochem Biophys. 2005 Jan 1;433(1):117-28. doi: 10.1016/j.abb.2004.08.015.
3
Fungal metabolic model for type I 3-methylglutaconic aciduria.I型3-甲基戊二酸尿症的真菌代谢模型。
J Biol Chem. 2004 Jul 30;279(31):32385-92. doi: 10.1074/jbc.M313044200. Epub 2004 Jun 4.
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4-Hydroxyphenylpyruvate dioxygenase as a drug discovery target.4-羟基苯丙酮酸双加氧酶作为药物研发靶点。
Drug News Perspect. 2003 Oct;16(8):493-6. doi: 10.1358/dnp.2003.16.8.829347.
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Fungal metabolic model for 3-methylcrotonyl-CoA carboxylase deficiency.3-甲基巴豆酰辅酶A羧化酶缺乏症的真菌代谢模型。
J Biol Chem. 2004 Feb 6;279(6):4578-87. doi: 10.1074/jbc.M310055200. Epub 2003 Nov 11.
6
Animal models reveal pathophysiologies of tyrosinemias.动物模型揭示了酪氨酸血症的病理生理学。
J Nutr. 2003 Jun;133(6 Suppl 1):2063S-2067S. doi: 10.1093/jn/133.6.2063S.
7
Quantitative analysis of the relative transcript levels of ABC transporter Atr genes in Aspergillus nidulans by real-time reverse transcription-PCR assay.通过实时逆转录聚合酶链反应分析对构巢曲霉中ABC转运蛋白Atr基因的相对转录水平进行定量分析。
Appl Environ Microbiol. 2002 Mar;68(3):1351-7. doi: 10.1128/AEM.68.3.1351-1357.2002.
8
PCR-mediated generation of a gene disruption construct without the use of DNA ligase and plasmid vectors.通过聚合酶链式反应（PCR）生成基因破坏构建体，无需使用DNA连接酶和质粒载体。
Nucleic Acids Res. 2002 Jan 15;30(2):E2. doi: 10.1093/nar/30.2.e2.
9
A fungal perspective on human inborn errors of metabolism: alkaptonuria and beyond.
Fungal Genet Biol. 2001 Oct;34(1):1-10. doi: 10.1006/fgbi.2001.1284.
10
Tyrosinemia: a review.酪氨酸血症：综述
Pediatr Dev Pathol. 2001 May-Jun;4(3):212-21. doi: 10.1007/s100240010146.

3型酪氨酸血症的真菌代谢模型：构巢曲霉中一种编码4-羟基苯丙酮酸双加氧酶的基因的分子特征

Fungal metabolic model for tyrosinemia type 3: molecular characterization of a gene encoding a 4-hydroxy-phenyl pyruvate dioxygenase from Aspergillus nidulans.

作者信息

da Silva Ferreira Márcia Eliana, Savoldi Marcela, Sueli Bonato Pierina, Goldman Maria Helena S, Goldman Gustavo H

机构信息

Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, São Paulo, Brazil.

出版信息

Eukaryot Cell. 2006 Aug;5(8):1441-5. doi: 10.1128/EC.00160-06.

DOI:10.1128/EC.00160-06
PMID:16896227
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1539140/
Abstract

Mutations in the human HPD gene (encoding 4-hydroxyphenylpyruvic acid dioxygenase) cause hereditary tyrosinemia type 3 (HT3). We deleted the Aspergillus nidulans homologue (hpdA). We showed that the mutant strain is not able to grow in the presence of phenylalanine and that it accumulates increased concentrations of tyrosine and 4-hydroxyphenylpyruvic acid, mimicking the human HT3 phenotype.

摘要

人类HPD基因（编码4-羟基苯丙酮酸双加氧酶）的突变会导致遗传性III型酪氨酸血症（HT3）。我们删除了构巢曲霉的同源基因（hpdA）。我们发现，该突变菌株在苯丙氨酸存在的情况下无法生长，并且积累了浓度升高的酪氨酸和4-羟基苯丙酮酸，模拟了人类HT3的表型。