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腺嘌呤和腺苷对嘌呤补救酶有缺陷的人类淋巴母细胞突变体有毒性。

Adenine and adenosine are toxic to human lymphoblast mutants defective in purine salvage enzymes.

作者信息

Hershfield M S, Snyder F F, Seegmiller J E

出版信息

Science. 1977 Sep 23;197(4310):1284-7. doi: 10.1126/science.197600.

DOI:10.1126/science.197600
PMID:197600
Abstract

Mutants deficient in adenosine kinase or adenine phosphoribosyltransferase activities were selected from the WI-L2 line of human lymphoblasts. The adenosine kinase-deficient mutant was still as sensitive as its parent to growth inhibition caused by adenosine deaminase was inhibited. Similarly, the adenine phosphoribosyltransferase mutant remained sensitive to growth inhibition caused by adenine. Thus, the toxicity of adenine and adenosine to human lymphoblasts is not mediated by nucleotides to which they may be converted.

摘要

从人淋巴母细胞WI-L2系中筛选出腺苷激酶或腺嘌呤磷酸核糖转移酶活性缺陷的突变体。腺苷激酶缺陷型突变体对腺苷脱氨酶抑制所引起的生长抑制仍与其亲本一样敏感。同样,腺嘌呤磷酸核糖转移酶突变体对腺嘌呤所引起的生长抑制仍敏感。因此,腺嘌呤和腺苷对人淋巴母细胞的毒性不是由它们可能转化而成的核苷酸介导的。

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Adenine and adenosine are toxic to human lymphoblast mutants defective in purine salvage enzymes.腺嘌呤和腺苷对嘌呤补救酶有缺陷的人类淋巴母细胞突变体有毒性。
Science. 1977 Sep 23;197(4310):1284-7. doi: 10.1126/science.197600.
2
Purine synthesis and excretion in mutants of the WI-L2 human lymphoblastoid line deficient in adenosine kinase (AK) and adenine phosphoribosyltransferase (APRT).腺苷激酶(AK)和腺嘌呤磷酸核糖转移酶(APRT)缺陷的WI-L2人淋巴母细胞系突变体中的嘌呤合成与排泄
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