| Product Includes | Product # | Quantity | Mol. Wt | Isotype/Source |
|---|---|---|---|---|
| Phospho-ATM (Ser1981) (D6H9) Rabbit mAb | 5883 | 20 µl | 350 kDa | Rabbit IgG |
| ATM (D2E2) Rabbit mAb | 2873 | 20 µl | 350 kDa | Rabbit IgG |
| Phospho-BRCA1 (Ser1524) Antibody | 9009 | 20 µl | 220 kDa | Rabbit |
| DNA-PKcs Antibody | 4602 | 20 µl | 450 kDa | Rabbit |
| Ku80 (C48E7) Rabbit mAb | 2180 | 20 µl | 86 kDa | Rabbit IgG |
| Mre11 (31H4) Rabbit mAb | 4847 | 20 µl | 81 kDa | Rabbit IgG |
| Phospho-p95/NBS1 (Ser343) Antibody | 3001 | 20 µl | 95 kDa | Rabbit |
| Rad50 Antibody | 3427 | 20 µl | 153 kDa | Rabbit |
| XLF Antibody | 2854 | 20 µl | 39 kDa | Rabbit |
| Anti-rabbit IgG, HRP-linked Antibody | 7074 | 100 µl | Goat |
Please visit cellsignal.com for individual component applications, species cross-reactivity, dilutions, protocols, and additional product information.
Description
The Double Strand Breaks (DSB) Repair Antibody Sampler Kit provides an economical means to investigate repair of double-strand DNA breaks within the cell. The kit contains primary and secondary antibodies to perform two western blots with each antibody.
Storage
Background
Double strand DNA breaks (DSB) in mammalian cells can be repaired by the related mechanisms of non-homologous end-joining (NHEJ) and homologous recombination (HR). A DNA-dependent protein kinase composed of DNA-binding subunits Ku70 and Ku86 and the DNA-PKcs catalytic subunit mediates NHEJ repair. The Ku heterodimer binds free DNA ends and recruits DNA-PKcs to the break (1). DNA-PKcs signals areas of DNA damage and recruits additional proteins, such as the Artemis exo- and endonuclease that processes and primes the damaged sequence (2,3). Following replacement DNA synthesis, a ligase complex composed of DNA ligase IV and XRCC4 joins the repaired ends. XRCC4-like factor (XLF) is an essential ligase-associated repair factor that promotes gap-filling during NHEJ (4). Homologous recombination utilizes aligned homologous sequences as a repair template. The MRN complex, composed of Mre11, Rad50, and nibrin (p95/NBS1), plays a critical role in sensing, processing and repairing breaks (5). MRN interacts with BRCA1 and CtIP to facilitate 5’ resection of DSB DNA to generate 3’ ssDNA ends necessary for repair (6). DNA-binding protein Mre11 exhibits exonuclease and endonuclease activity and is largely responsible for ssDNA end processing (7). Interaction between the MRN complex and ATM kinase promotes association between the kinase and its substrates and likely leads to ATM activation (8). ATM acts a central controller of the cell cycle checkpoint by phosphorylating multiple targets, including c-Abl, BRCA1 and p95/NSB1. Activated c-Abl phosphorylates Rad52, which promotes Rad51 binding to ssDNA and subsequent annealing of ssDNA (7).
- Gottlieb, T.M. and Jackson, S.P. (1993) Cell 72, 131-42.
- Franco, S. et al. (2008) J Exp Med 205, 557-64.
- Collis, S.J. et al. (2005) Oncogene 24, 949-61.
- Akopiants, K. et al. (2009) Nucleic Acids Res 37, 4055-62.
- Williams, R.S. et al. (2007) Biochem Cell Biol 85, 509-20.
- Chen, L. et al. (2008) J Biol Chem 283, 7713-20.
- Czornak, K. et al. (2008) J Appl Genet 49, 383-96.
- Lee, J.H. and Paull, T.T. (2007) Oncogene 26, 7741-8.
Background References
Trademarks and Patents
Limited Uses
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