| 货号 | 4895S |
| 反应种属 | Human/Mouse/Rat/Monkey |
| 来源宿主 | Rabbit |
| 应用 | W/IP/IHC-P/IHC-F |
| 使用方法 | WB(1:1000) IP (1:100) IHC-P (1:500) IHC-F (1:1000) |
| 供应商 | CST |
| 背景 | 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).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)。 |
| 存放说明 | -20C |
| 计算分子量 | 81 |
Western blot analysis of extracts from Jurkat (human), L929 (mouse), Neuro-2a (mouse) and C6 (rat) cells, using Mre11 Antibody. | |
Immunohistochemical analysis of paraffin-embedded human colon carcinoma, showing nuclear localization, using Mre11 Antibody. | |
Immunohistochemical analysis of paraffin-embedded human breast carcinoma, using Mre11 Antibody in the presence of control peptide (left) or Mre11 Blocking Peptide #1035 (right). | |
Immunohistochemical analysis of H1650 xenograft, using Mre11 Antibody. |
