Cell Signaling Technology

Product Pathways - DNA Damage

Phospho-ATM (Ser1981) (D6H9) Rabbit mAb #5883

ATM   ATR   DNA-PK   PIKK Family   sc-47739  

No. Size Price
5883S 100 µl ( 10 western blots ) ¥4,050.00 现货查询 购买询价 防伪查询
5883T 20 µl ( 2 western blots ) ¥1,500.00 现货查询 购买询价 防伪查询
5883 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 350 Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,


Species predicted to react based on 100% sequence homology: Monkey, Bovine, Pig, Horse,

Specificity / Sensitivity

Phospho-ATM (Ser1981) (D6H9) Rabbit mAb recognizes endogenous levels of ATM protein only when phosphorylated at Ser1981. Phospho-ATM (Ser1981) (D6H9) Rabbit mAb能够识别内源性的丝氨酸(1981位点)磷酸化的ATM蛋白。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser1981 of human ATM protein. 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

Western blot analysis of extracts from 293 cells, untreated or UV-treated (100 mJ, 4 hr recovery), using Phospho-ATM (Ser1981) (D6H9) Rabbit mAb (upper) or ATM (D2E2) Rabbit mAb #2873 (lower). Western blot方法检测细胞提取物:未处理和紫外处理(100mJ,4小时恢复)的293细胞。分别使用Phospho-ATM (Ser1981) (D6H9) Rabbit mAb (上图)和ATM (D2E2) Rabbit mAb #2873 (下图)检测ATM蛋白水平。


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.

Application References

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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.

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