Xi Tong, Jones Irene M, Mohrenweiser Harvey W
Biology and Biotechnology Research Program, Lawrence Livermore National Laboratory, Livermore, CA 94550, USA.
Genomics. 2004 Jun;83(6):970-9. doi: 10.1016/j.ygeno.2003.12.016.
Over 520 different amino acid substitution variants have been previously identified in the systematic screening of 91 human DNA repair genes for sequence variation. Two algorithms were employed to predict the impact of these amino acid substitutions on protein activity. Sorting Intolerant from Tolerant (SIFT) classified 226 of 508 variants (44%) as "Intolerant." Polymorphism Phenotyping (PolyPhen) classed 165 of 489 amino acid substitutions (34%) as "Probably or possibly damaging." Another 9-15% of the variants were classed as "Potentially intolerant or damaging." The results from the two algorithms are highly associated, with concordance in predicted impact observed for approximately 62% of the variants. Twenty-one to thirty-one percent of the variant proteins are predicted to exhibit reduced activity by both algorithms. These variants occur at slightly lower individual allele frequency than do the variants classified as "Tolerant" or "Benign." Both algorithms correctly predicted the impact of 26 functionally characterized amino acid substitutions in the APE1 protein on biochemical activity, with one exception. It is concluded that a substantial fraction of the missense variants observed in the general human population are functionally relevant. These variants are expected to be the molecular genetic and biochemical basis for the associations of reduced DNA repair capacity phenotypes with elevated cancer risk.
此前在对91个人类DNA修复基因进行序列变异的系统筛查中,已鉴定出超过520种不同的氨基酸替代变体。采用了两种算法来预测这些氨基酸替代对蛋白质活性的影响。从耐受中筛选不耐受(SIFT)将508个变体中的226个(44%)分类为“不耐受”。多态性表型分析(PolyPhen)将489个氨基酸替代中的165个(34%)分类为“可能或可能有害”。另外9%-15%的变体被分类为“潜在不耐受或有害”。两种算法的结果高度相关,约62%的变体在预测影响上具有一致性。两种算法都预测21%-31%的变体蛋白活性会降低。这些变体的个体等位基因频率略低于被分类为“耐受”或“良性”的变体。两种算法都正确预测了APE1蛋白中26个功能特征化的氨基酸替代对生化活性的影响,只有一个例外。得出的结论是,在普通人群中观察到的相当一部分错义变体在功能上是相关的。这些变体有望成为DNA修复能力降低表型与癌症风险升高之间关联的分子遗传和生化基础。