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Organic aciduria in the riboflavin-deficient rat.

作者信息

Goodman S I

出版信息

Am J Clin Nutr. 1981 Nov;34(11):2434-7. doi: 10.1093/ajcn/34.11.2434.

DOI:10.1093/ajcn/34.11.2434
PMID:6895440
Abstract
摘要

相似文献

1
Organic aciduria in the riboflavin-deficient rat.核黄素缺乏大鼠中的有机酸尿症
Am J Clin Nutr. 1981 Nov;34(11):2434-7. doi: 10.1093/ajcn/34.11.2434.
2
Altered acyl-CoA metabolism in riboflavin deficiency.核黄素缺乏时酰基辅酶A代谢的改变。
Biochim Biophys Acta. 1989 Dec 18;1006(3):335-43. doi: 10.1016/0005-2760(89)90021-0.
3
FAD-dependent regulation of transcription, translation, post-translational processing, and post-processing stability of various mitochondrial acyl-CoA dehydrogenases and of electron transfer flavoprotein and the site of holoenzyme formation.黄素腺嘌呤二核苷酸（FAD）依赖的对各种线粒体酰基辅酶A脱氢酶、电子传递黄素蛋白的转录、翻译、翻译后加工以及加工后稳定性的调节作用，以及全酶形成位点。
J Biol Chem. 1992 Sep 5;267(25):17925-32.
4
Biochemical studies in a patient with defects in the metabolism of acyl-CoA and sarcosine: another possible case of glutaric aciduria type II.一名患有酰基辅酶A和肌氨酸代谢缺陷患者的生化研究：另一个可能的II型戊二酸尿症病例
J Inherit Metab Dis. 1980;3(3):67-72. doi: 10.1007/BF02312527.
5
Glutaric aciduria type II: evidence for a defect related to the electron transfer flavoprotein or its dehydrogenase.II型戊二酸尿症：与电子传递黄素蛋白或其脱氢酶相关缺陷的证据。
Pediatr Res. 1984 Jul;18(7):663-7. doi: 10.1203/00006450-198407000-00020.
6
Mechanism of action of glutaryl-CoA and butyryl-CoA dehydrogenases. Purification of glutaryl-CoA dehydrogenase.戊二酰辅酶A和丁酰辅酶A脱氢酶的作用机制。戊二酰辅酶A脱氢酶的纯化。
Biochemistry. 1981 Mar 17;20(6):1481-90. doi: 10.1021/bi00509a012.
7
Catalytic defect of medium-chain acyl-coenzyme A dehydrogenase deficiency. Lack of both cofactor responsiveness and biochemical heterogeneity in eight patients.中链酰基辅酶A脱氢酶缺乏症的催化缺陷。八例患者缺乏辅因子反应性和生化异质性。
J Clin Invest. 1985 Sep;76(3):963-9. doi: 10.1172/JCI112096.
8
Effects of riboflavin deficiency and clofibrate treatment on the five acyl-CoA dehydrogenases in rat liver mitochondria.核黄素缺乏与氯贝丁酯治疗对大鼠肝脏线粒体中五种酰基辅酶A脱氢酶的影响。
Biochem J. 1988 Sep 1;254(2):477-81. doi: 10.1042/bj2540477.
9
Improved assay of glutaryl-CoA dehydrogenase in cultured cells and liver: application to glutaric aciduria type I.培养细胞和肝脏中戊二酰辅酶A脱氢酶检测方法的改进：应用于I型戊二酸尿症
Clin Chim Acta. 1983 Mar 28;129(1):91-7. doi: 10.1016/0009-8981(83)90155-9.
10
Specific glutaryl-CoA dehydrogenating activity is deficient in cultured fibroblasts from glutaric aciduria patients.戊二酸尿症患者培养的成纤维细胞中特定的戊二酰辅酶A脱氢酶活性缺乏。
J Clin Invest. 1984 Mar;73(3):778-84. doi: 10.1172/JCI111271.

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2
First report of paternal uniparental disomy of chromosome 8 with mutation in Brown-vialetto-van laere syndrome type 2 and an analysis of genotype-phenotype correlations.8号染色体父源单亲二体合并2型Brown-Vialetto-van Laere综合征突变的首例报告及基因型-表型相关性分析
Front Genet. 2022 Sep 15;13:977914. doi: 10.3389/fgene.2022.977914. eCollection 2022.
3
Dietary Reference Values for riboflavin.
核黄素的膳食参考值。
EFSA J. 2017 Aug 7;15(8):e04919. doi: 10.2903/j.efsa.2017.4919. eCollection 2017 Aug.
4
Impaired riboflavin transport due to missense mutations in SLC52A2 causes Brown-Vialetto-Van Laere syndrome.由于 SLC52A2 中的错义突变导致核黄素转运受损会引起 Brown-Vialetto-Van Laere 综合征。
J Inherit Metab Dis. 2012 Nov;35(6):943-8. doi: 10.1007/s10545-012-9513-y. Epub 2012 Aug 3.
5
Brown-Vialetto-Van Laere and Fazio Londe syndrome is associated with a riboflavin transporter defect mimicking mild MADD: a new inborn error of metabolism with potential treatment.Brown-Vialetto-Van Laere 与 Fazio Londe 综合征与一种类似轻度 MADD 的核黄素转运蛋白缺陷有关：一种具有潜在治疗方法的新的先天性代谢缺陷。
J Inherit Metab Dis. 2011 Feb;34(1):159-64. doi: 10.1007/s10545-010-9242-z. Epub 2010 Nov 26.
6
Hepatic peroxisomal and mitochondrial fatty acid oxidation in the riboflavin-deficient rat.核黄素缺乏大鼠肝脏中过氧化物酶体和线粒体的脂肪酸氧化
Biochem J. 1985 Aug 1;229(3):717-21. doi: 10.1042/bj2290717.
7
Acyl-CoA dehydrogenase activity in the riboflavin-deficient rat. Effects of starvation.核黄素缺乏大鼠的酰基辅酶A脱氢酶活性。饥饿的影响。
Biochem J. 1987 Jun 1;244(2):387-91. doi: 10.1042/bj2440387.
8
Effects of riboflavin deficiency and clofibrate treatment on the five acyl-CoA dehydrogenases in rat liver mitochondria.核黄素缺乏与氯贝丁酯治疗对大鼠肝脏线粒体中五种酰基辅酶A脱氢酶的影响。
Biochem J. 1988 Sep 1;254(2):477-81. doi: 10.1042/bj2540477.
9
Products and intermediates of the beta-oxidation of [U-14C]hexadecanedionoyl-mono-CoA by rat liver peroxisomes and mitochondria.大鼠肝脏过氧化物酶体和线粒体对[U-14C]十六烷二酰单辅酶A进行β-氧化的产物和中间体。
Biochem J. 1991 Jan 1;273(Pt 1)(Pt 1):205-10. doi: 10.1042/bj2730205.