Reddy Prasad T, Jaruga Pawel, Nelson Bryant C, Lowenthal Mark S, Jemth Ann-Sofie, Loseva Olga, Coskun Erdem, Helleday Thomas, Dizdaroglu Miral
Institute for Bioscience and Biotechnology Research, National Institute of Standards and Technology and the University of Maryland, Rockville, Maryland, USA.
Biochemical Measurement Division, National Institute of Standards and Technology, Gaithersburg, Maryland, USA.
Methods Enzymol. 2016;566:305-32. doi: 10.1016/bs.mie.2015.06.044. Epub 2015 Jul 26.
Oxidatively induced DNA damage is caused in living organisms by a variety of damaging agents, resulting in the formation of a multiplicity of lesions, which are mutagenic and cytotoxic. Unless repaired by DNA repair mechanisms before DNA replication, DNA lesions can lead to genomic instability, which is one of the hallmarks of cancer. Oxidatively induced DNA damage is mainly repaired by base excision repair pathway with the involvement of a plethora of proteins. Cancer tissues develop greater DNA repair capacity than normal tissues by overexpressing DNA repair proteins. Increased DNA repair in tumors that removes DNA lesions generated by therapeutic agents before they became toxic is a major mechanism in the development of therapy resistance. Evidence suggests that DNA repair capacity may be a predictive biomarker of patient response. Thus, knowledge of DNA-protein expressions in disease-free and cancerous tissues may help predict and guide development of treatments and yield the best therapeutic response. Our laboratory has developed methodologies that use mass spectrometry with isotope dilution for the measurement of expression of DNA repair proteins in human tissues and cultured cells. For this purpose, full-length (15)N-labeled analogs of a number of human DNA repair proteins have been produced and purified to be used as internal standards for positive identification and accurate quantification. This chapter describes in detail the protocols of this work. The use of (15)N-labeled proteins as internal standards for the measurement of several DNA repair proteins in vivo is also presented.
氧化诱导的DNA损伤在生物体内由多种损伤因子引起,导致形成多种损伤,这些损伤具有致突变性和细胞毒性。除非在DNA复制前通过DNA修复机制进行修复,否则DNA损伤会导致基因组不稳定,这是癌症的标志之一。氧化诱导的DNA损伤主要通过碱基切除修复途径进行修复,涉及大量蛋白质。癌症组织通过过度表达DNA修复蛋白,比正常组织具有更强的DNA修复能力。肿瘤中DNA修复增加,在治疗剂产生毒性之前去除其产生的DNA损伤,这是治疗抗性发展的主要机制。有证据表明,DNA修复能力可能是患者反应的预测生物标志物。因此,了解无病组织和癌组织中DNA-蛋白质的表达情况可能有助于预测和指导治疗的发展,并产生最佳的治疗反应。我们实验室已经开发出利用同位素稀释质谱法来测量人类组织和培养细胞中DNA修复蛋白表达的方法。为此,已经生产并纯化了多种人类DNA修复蛋白的全长(15)N标记类似物,用作阳性鉴定和准确定量的内标。本章详细描述了这项工作的方案。还介绍了使用(15)N标记蛋白作为内标在体内测量几种DNA修复蛋白的方法。