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Azaguanine-resistance as a manifestation of a new form of metabolic overproduction of uric acid.

作者信息

Benke P J, Herrick N

出版信息

Am J Med. 1972 Apr;52(4):547-55. doi: 10.1016/0002-9343(72)90046-0.

DOI:10.1016/0002-9343(72)90046-0
PMID:5017247
Abstract
摘要

相似文献

1
Azaguanine-resistance as a manifestation of a new form of metabolic overproduction of uric acid.
Am J Med. 1972 Apr;52(4):547-55. doi: 10.1016/0002-9343(72)90046-0.
2
In vitro effects of magnesium ions on mutant cells from patients with the Lesch-Nyhan syndrome.镁离子对莱施-奈恩综合征患者突变细胞的体外作用。
N Engl J Med. 1973 Aug 30;289(9):446-50. doi: 10.1056/NEJM197308302890903.
3
Aetiology of gout.痛风的病因
Scott Med J. 1973;18:Suppl 1:222-31. doi: 10.1177/00369330730180s102.
4
Hypoxanthine-guanine phosphoribosyltransferase variant associated with accelerated purine synthesis.与嘌呤合成加速相关的次黄嘌呤-鸟嘌呤磷酸核糖转移酶变体
J Clin Invest. 1973 Sep;52(9):2234-40. doi: 10.1172/JCI107409.
5
Erythrocyte adenine phosphoribosyltransferase in the Lesch-Nyhan syndrome.莱施-奈恩综合征中的红细胞腺嘌呤磷酸核糖基转移酶
Isr J Med Sci. 1973 Nov-Dec;9(11):1553-8.
6
Genetic aspects of gout.痛风的遗传学方面
Annu Rev Med. 1974;25(0):15-28. doi: 10.1146/annurev.me.25.020174.000311.
7
Gout with purine overproduction due to increased phosphoribosylpyrophosphate synthetase activity.由于磷酸核糖焦磷酸合成酶活性增加导致嘌呤产生过多的痛风。
Am J Med. 1973 Aug;55(2):232-42. doi: 10.1016/0002-9343(73)90174-5.
8
An atypical case of hypoxanthine-guanine phosphoribosyltransferase deficiency (Lesch-Nyhan syndrome). II. Genetic studies.
Clin Genet. 1973;4(4):353-9. doi: 10.1111/j.1399-0004.1973.tb01931.x.
9
Alterations in the activity of hypoxanthine and adenine phosphoribosyltransferase in patients with hyperuricaemia and gout.
Q J Med. 1971 Oct;40(160):574-5.
10
Selected aspects of the aetiology, pathogenesis and treatment of disorders of purine metabolism.嘌呤代谢紊乱的病因、发病机制及治疗的某些方面
Mod Trends Rheumatol. 1971;2:299-322.

引用本文的文献

1
Partial deficiency of hypoxanthine-guanine phosphoribosyltransferase with reduced affinity for PP-ribose-P in four related males with gout.四名痛风相关男性中次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶部分缺乏,对磷酸核糖焦磷酸(PP - ribose - P)的亲和力降低。
Hum Genet. 1984;67(1):18-22. doi: 10.1007/BF00270552.
2
The spontaneous azaguanine-resistant mutants of diploid human fibroblasts.二倍体人成纤维细胞的自发氮鸟嘌呤抗性突变体。
Humangenetik. 1972;16(1):87-110. doi: 10.1007/BF00393992.
3
Expression of purine overproduction in a series of 8-azaguanine-resistant diploid human lymphoblast lines.
一系列对8-氮杂鸟嘌呤耐药的二倍体人淋巴母细胞系中嘌呤过度产生的表达。
Proc Natl Acad Sci U S A. 1974 Jul;71(7):2679-83. doi: 10.1073/pnas.71.7.2679.
4
Hypoxanthine-guanine phosphoribosyltransferase variant associated with accelerated purine synthesis.与嘌呤合成加速相关的次黄嘌呤-鸟嘌呤磷酸核糖转移酶变体
J Clin Invest. 1973 Sep;52(9):2234-40. doi: 10.1172/JCI107409.
5
Clinical and biochemical observations on three cases of hypoxanthine-guanine phosphoribosyltransferase deficiency.三例次黄嘌呤-鸟嘌呤磷酸核糖转移酶缺乏症的临床与生化观察
Ann Rheum Dis. 1975 Jun;34(3):249-55. doi: 10.1136/ard.34.3.249.
6
Hypoxanthine phosphoribosyltransferase activity in intact fibroblasts from patients with X-linked hyperuricemia.X连锁高尿酸血症患者完整成纤维细胞中的次黄嘌呤磷酸核糖基转移酶活性
J Clin Invest. 1976 Jun;57(6):1600-5. doi: 10.1172/JCI108430.
7
Molecular and tissue-specific heterogeneity in HPRT deficiency.次黄嘌呤磷酸核糖转移酶缺乏症中的分子和组织特异性异质性。
Biochem Genet. 1978 Dec;16(11-12):1187-202. doi: 10.1007/BF00484539.