| Product Includes | Product # | Quantity | Mol. Wt | Isotype/Source |
|---|---|---|---|---|
| Phospho-Chk2 (Thr68) (E8Q1A) Rabbit mAb | 82263 | 20 µl | 62 kDa | Rabbit IgG |
| Chk2 (D9C6) Rabbit mAb | 6334 | 20 µl | 62 kDa | Rabbit IgG |
| Phospho-p53 (Ser15) (E9Y4U) Rabbit mAb | 82530 | 20 µl | 53 kDa | Rabbit IgG |
| p53 (7F5) Rabbit mAb | 2527 | 20 µl | 53 kDa | Rabbit IgG |
| Rad50 (E3I8K) Rabbit mAb | 86225 | 20 µl | 153 kDa | Rabbit IgG |
| Phospho-p95/NBS1 (Ser343) Antibody | 3001 | 20 µl | 95 kDa | Rabbit |
| p95/NBS1 (E8M3Q) XP® Rabbit mAb | 81234 | 20 µl | 95 kDa | Rabbit IgG |
| Anti-rabbit IgG, HRP-linked Antibody | 7074 | 100 µl | Goat | |
| Phospho-Rad50 (Ser635) (F5H8B) Rabbit mAb | 99215 | 20 µl | 153 kDa | Rabbit IgG |
Please visit cellsignal.com for individual component applications, species cross-reactivity, dilutions, protocols, and additional product information.
Description
The ATM Substrates Antibody Sampler Kit provides an economical means to evaluate the signaling of ATM to downstream substrates. The kit contains enough primary and secondary antibodies to perform two Western blot experiments per primary antibody.
Storage
Background
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).
Background References
Trademarks and Patents
Limited Uses
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