Simple Western™ analysis of lysates (0.1 mg/mL) from 293 cells treated with UV (100 mJ/cm2; 2 Hour Recovery) using Phospho-ATM (Ser1981) (D25E5) Rabbit mAb #13050. The virtual lane view (left) shows the target band (as indicated) at 1:10 and 1:50 dilutions of primary antibody. The corresponding electropherogram view (right) plots chemiluminescence by molecular weight along the capillary at 1:10 (blue line) and 1:50 (green line) dilutions of primary antibody. This experiment was performed under reducing conditions on the Jess™ Simple Western instrument from ProteinSimple, a BioTechne brand, using the 66 - 440 kDa separation module.
| Cat. # | Size | Qty. | Price |
|---|---|---|---|
| 31068S | 1 Kit |
|
| Product Includes | Quantity | Reactivity | MW(kDa) | Isotype | |
|---|---|---|---|---|---|
| ATM (D2E2) Rabbit mAb 2873 | 100 µl | H M | 350 | Rabbit IgG | |
| Phospho-ATM (Ser1981) (D25E5) Rabbit mAb 13050 | 100 µl | H | 350 | Rabbit IgG |
Product Information
ATM (ataxia telangiectasia mutated kinase) is a serine/threonine protein kinase best known for its role in DNA repair signaling in response to DNA double-strand breaks (DSBs). When DSBs occur, the MRE11:RAD50:NBS1 (MRN) sensor complex recruits ATM to sites of DNA damage. ATM then signals to numerous effector proteins, leading to cellular responses including regulation of DNA repair, cell cycle progression, apoptosis, senescence, gene transcription. Along with ATR, DNA-PKcs, SMG1 and mTOR, ATM is a member of the PI3K-like protein kinase (PIKK) family. PIKK family members typically function in response to various types of cellular stress. Substrates of ATM are numerous, and include CHK2, AKT, p53, BRCA1 and DNA-PK (reviewed in 1,3). Inactive ATM exists as a homodimer. In response to DSBs, ATM undergoes autophosphorylation in trans at Ser1981, which leads to dissociation of the complex to become an active monomer (2). Functional DNA repair pathways are important in cellular homeostasis, and defects in these pathways cause genomic instability, which can lead to tumorigenesis (3). Inactivation of ATM results in ataxia telangiectasia (AT), a neurodegenerative disease characterized by predisposition to cancer (4).
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