Phospho-ATM (Ser1981) (10H11.E12) Mouse mAb
货号：
4526L 基本售价：
9300.0 元 规格：
-
产品信息
概述| 货号 | 4526L |
| 反应种属 | Human |
| 来源宿主 | Mouse |
| 应用 | W |
| 使用方法 | WB(1:1000) |
性能| 供应商 | CST |
| 背景 | Ataxia telangiectasia mutated kinase (ATM) is a serine/threonine kinase that regulates cell cycle checkpoints and DNA repair (1). Activation of ATM by autophosphorylation on Ser1981 occurs in response to exposed DNA double stranded breaks. ATM kinase regulates a number of proteins involved in cell cycle checkpoint control, apoptosis, and DNA repair. Known substrates include p53, Chk2, Chk1, CtIP, 4E-BP1, BRCA1, RPA3, H2A.X, SMC1, FANCD2, Rad17, Artemis, Nbs1, and the I-2 regulatory subunit of PP1 (1,2). Mutations in the corresponding ATM gene result in ataxia telangiectasia (AT), an autosomal recessive disease characterized by uncoordinated muscle movement and neurodegeneration. Cells from AT patients display defective DNA damage-induced checkpoint activation, sensitivity to radiation, and a higher frequency of chromosome breakage (3,4).共济失调毛细血管扩张症突变蛋白激酶(ATM)是一种丝氨酸/苏氨酸激酶，能够调节细胞周期检验点和DNA修复(1)。 丝氨酸(1981位)自体磷酸化激活ATM的发生响应裸露的DNA双链断裂。 ATM激酶调节许多蛋白，涉及细胞周期检验点的控制、细胞凋亡和DNA修复。已知的ATM底物包括P53，CHK2，CHK1，CtIP，4E-BP1，BRCA1，RPA3，H2A.X，SMC1，FANCD2，Rad17，Artemis，Nbs1和PP1的I-2调节亚基(1,2)。ATM基因突变可导致共济失调毛细血管扩张症(AT)，一种常染色体隐性遗传病，该病特点是不协调的肌肉运动和神经退化。来自AT病人的细胞显示有缺陷的DNA损伤诱导检验点激活，对放射的敏感性和频率较高的染色体断裂(3,4)。 |
| 存放说明 | -20C |
| 计算分子量 | 350 |
参考图片ATM (D2E2) Rabbit mAb #2873 analysis of extracts from M059J cells, untreated, treated with doxorubicin, or treated with bleomycin, using Phospho-ATM (Ser1981) (10H11.E12) Mouse mAbWestern blot方法检测M059J细胞提取物：分别是未处理、阿霉素处理或博来霉素处理的细胞，使用的抗体为Phospho-ATM (Ser1981) (10H11.E12) Mouse mAb。 |
