Mre11 Antibody能够检测内源性Mre11 homologue A (Mre11A)蛋白,可能会与Mre11 homologue B (Mre11B)发生交叉反应。该多克隆抗体是由合成的人源的针对MrellA蛋白赖氨酸(496位)的肽段免疫动物,利用A蛋白和多肽亲和层析方法纯化生产的。Mre11最初在酿酒酵母(其突变体在减数分裂重组过程中是有缺陷的)的基因筛选中被描述(1),它是多亚基核酸酶(MRN,由Mre11, Rad50和Nbs1组成)的关键组成部分(2,3)。MRN复合体在感知、处理和修复DNA双链断裂过程中起重要作用。其缺陷会导致基因组不稳定,端粒缩短,减数分裂异常和过敏性DNA损伤(4)。在共济失调毛细血管扩张疾病(ATLD)中已经发现了Mre11的亚等位基因突变,其表型类似于引起共济失调毛细血管扩张症(A-T)的来自ATM的突变,包括人类恶性肿瘤的易感性(5)。ATLD带来的细胞水平的不良后果主要有染色体不稳定性和响应DNA损伤的内-S期和G2/M期检验点缺陷。MRN复合体能够直接激活DNA断裂的ATM检验点激酶(6)。
Mre11 Antibody detects endogenous levels of Mre11 homologue A (Mre11A). The antibody may cross-react with Mre11 homologue B (Mre11B).
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys496 of human Mre11A. Antibodies are purified by protein A and peptide affinity chromatography.
Background
Mre11, originally described in genetic screens from the yeast Saccharomyces cerevisiae in which mutants were defective in meiotic recombination (1), is a central part of a multisubunit nuclease composed of Mre11, Rad50 and Nbs1 (MRN) (2,3). The MRN complex plays a critical role in sensing, processing and repairing DNA double strand breaks. Defects lead to genomic instability, telomere shortening, aberrant meiosis and hypersensitivity to DNA damage (4). Hypomorphic mutations of Mre11 are found in ataxia-telangiectasia-like disease (ATLD), with phenotypes similar to mutations in ATM that cause ataxia-telangiectasia (A-T), including a predisposition to malignancy in humans (5). Cellular consequences of ATLD include chromosomal instability and defects in the intra-S phase and G2/M checkpoints in response to DNA damage. The MRN complex may directly activate the ATM checkpoint kinase at DNA breaks (6).