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着色性干皮病d互补组中无嘌呤SV40 DNA的存活情况。

Survival of apurinic SV40 DNA in the d-complementation group of xeroderma pigmentosum.

作者信息

Kudrna R D, Smith J, Linn S, Penhoet E E

出版信息

Mutat Res. 1979 Aug;62(1):173-81. doi: 10.1016/0027-5107(79)90230-6.

Abstract

The survival of depurinated Form I SV40 DNA was studied in normal human fibroblasts and in D-complementation Xeroderma pigmentosum (XP) fibroblasts. Survival was measured with an infective center assay. Heat-acid and methyl methanesulfonate (MMS) were used as depurinating agents. After 3 hrs of depurination by heat--acid treatment, infectivity in normal cells was less than 15% of the controls compared to more than 50% for the XP D cell strains. Similar results were obtained with MMS-treated DNA. These results are contrary to expectation since apurinic endonuclease activity, which is presumed to be involved in the repair of apurinic sites, is much lower in XP D cell strains than in normal cell strains. Our results indicate that another mechanism for the repair of apurinic sites could exist.

摘要

研究了脱嘌呤的I型SV40 DNA在正常人成纤维细胞和D互补型着色性干皮病(XP)成纤维细胞中的存活情况。通过感染中心试验来测定存活率。热酸和甲基磺酸甲酯(MMS)用作脱嘌呤剂。经过热酸处理脱嘌呤3小时后,正常细胞中的感染性不到对照的15%,而XP D细胞株则超过50%。用MMS处理的DNA也得到了类似结果。这些结果与预期相反,因为据推测参与脱嘌呤位点修复的脱嘌呤内切酶活性在XP D细胞株中比在正常细胞株中低得多。我们的结果表明可能存在另一种修复脱嘌呤位点的机制。

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