Cell Signaling Technology

Product Pathways - DNA Damage

Phospho-ATM (Ser1981) (10H11.E12) Mouse mAb #4526

A-T   ataxia telangiectasia mutated   ATM   ATR   DNA-PK   PIKK Family   sc-47739  

No. Size Price
4526L 300 µl ( 30 western blots ) ¥8,792.00 现货查询 购买询价
4526S 100 µl ( 10 western blots ) ¥3,900.00 现货查询 购买询价
4526T 20 µl ( 2 western blots ) ¥1,300.00 现货查询 购买询价
4526 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 350 Mouse

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,

Specificity / Sensitivity

Phospho-ATM (Ser1981) (10H11.E12) Mouse mAb detects endogenous levels of ATM only when phosphorylated at Ser1981. Phospho-ATM (Ser1981) (10H11.E12)能够检测内源性的丝氨酸(1981位点)磷酸化的ATM蛋白。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues around Ser1981 of human ATM. 该单克隆抗体是由合成的人源的针对ATM蛋白丝氨酸(1981位)磷酸化肽段免疫动物而生产的。

Western Blotting

Western Blotting

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 mAb Western 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。

Background

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)。

  1. Lee, J.H. and Paull, T.T. (2007) Oncogene 26, 7741-8.
  2. Tang, X. et al. (2008) Mol Cell Biol 28, 2559-66.
  3. Shiloh, Y. (1997) Annu Rev Genet 31, 635-62.
  4. Petrini, J.H. (2000) Curr Opin Cell Biol 12, 293-6.

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For Research Use Only. Not For Use In Diagnostic Procedures.

Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.

This product is sold under license, U.S. Patent Publication numbers 2003/0077661 and 2003/0157572, from St. Jude Childrens Research Hospital.

Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.

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