特别地，在非蛋白质编码部分选择如何工作，选择丢弃什么样的变异：少数常见基因影响小或者许多罕见基因影响大？
In particular, how does it work on the non-protein-coding parts, and what kinds of variation does it leave behind: a few common genes with small effects or many rare genes with large effects?
这一细节让他们作出结论：可能是遗传获得的非编码DNA序列、而不是基因变异才使得最大部分的转录因子结合位置发生变化。
This detail led them to conclude that inherited non-coding DNA sequences – not mutations in genes – may drive the lion's share of differences in where transcription factors attach.
特别地，在非蛋白质编码部分选择如何工作，选择丢弃什么样的变异：少数常见基因影响小或者许多罕见基因影响大？
In particular how does it work on the non-protein-coding parts and what kinds of variation does it leave behind: a few common genes with small effects or many rare genes with large effects?
目的研究柯萨奇B组3型病毒（CVB3）中国分离株结构蛋白VP4、非结构蛋白3D基因序列及变异性。
Objective To investigate the sequence and variation of VP4 and 3D gene of a coxsackievirus B3 Chinese isolate(CVB3-Chi).
由于核苷酸切除修复、药物转运和药物代谢通路在铂金药物功能中的重要性，这篇综述重点总结了这些通路中的基因表达和非癌细胞DNA变异与铂金疗效的关系。
We focused on several key pathways, including nucleotide excision repair, drug transport and metabolism. Both expression and germline DNA variation were evaluated in these key pathways.
Pfizer的crizotinib专门攻击某种基因转录的蛋白，只有少于5%的非小细胞肺癌患者具有这种基因。 Roche的vemurafenib通过阻断基因B-RAF的变异体抵抗晚期黑色素瘤。
Pfizer's crizotinib attacks a protein encoded by a gene found in fewer than 5% of patients with non-small-cell lung cancer.
Pfizer的crizotinib专门攻击某种基因转录的蛋白，只有少于5%的非小细胞肺癌患者具有这种基因。 Roche的vemurafenib通过阻断基因B-RAF的变异体抵抗晚期黑色素瘤。
Pfizer's crizotinib attacks a protein encoded by a gene found in fewer than 5% of patients with non-small-cell lung cancer.
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