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1 rom DNA suggests an age-dependent decline in 3-methyladenine DNA glycosylase, a BER enzyme responsibl
6 UC with increases in the DNA repair enzymes 3-methyladenine DNA glycosylase and apurinic/apyrimidini
7 base excision-repair enzymes, AAG, the major 3-methyladenine DNA glycosylase, and APE1, the major apu
9 Methylpurine-DNA glycosylases (MPG proteins, 3-methyladenine-DNA glycosylases) excise numerous damage
10 nt of the DNA with uracil-DNA glycosylase or 3-methyladenine DNA glycosylase failed to reveal additio
12 NA excision repair genes (including the MAG1 3-methyladenine DNA glycosylase gene) and a large select
18 is approximately 0.3 in strains deficient in 3-methyladenine DNA glycosylases I and II, FAPY DNA glyc
19 e DNA glycosylase (AAG) and Escherichia coli 3-methyladenine DNA glycosylase II (AlkA) bind tightly t
23 monofunctional DNA glycosylase AlkA (E. coli 3-methyladenine-DNA glycosylase II) reveals a large hydr
26 n between ERalpha and the DNA repair protein 3-methyladenine DNA glycosylase (MPG) thereby providing
29 study was made possible by the generation of 3-methyladenine DNA glycosylase null mutant cells by tar
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