| Product Includes | Product # | Quantity | Mol. Wt | Isotype/Source |
|---|---|---|---|---|
| Phospho-cdc2 (Tyr15) (10A11) Rabbit mAb | 4539 | 20 µl | 34 kDa | Rabbit |
| Phospho-Chk1 (Ser345) (133D3) Rabbit mAb | 2348 | 20 µl | 56 kDa | Rabbit IgG |
| Phospho-Chk2 (Thr68) (C13C1) Rabbit mAb | 2197 | 20 µl | 62 kDa | Rabbit IgG |
| Phospho-Rb (Ser807/811) (D20B12) XP® Rabbit mAb | 8516 | 20 µl | 110 kDa | Rabbit IgG |
| Phospho-Rb (Ser795) Antibody | 9301 | 20 µl | 110 kDa | Rabbit |
| Phospho-p53 (Ser15) (16G8) Mouse mAb | 9286 | 20 µl | 53 kDa | Mouse IgG1 |
| Anti-rabbit IgG, HRP-linked Antibody | 7074 | 100 µl | Goat | |
| Anti-mouse IgG, HRP-linked Antibody | 7076 | 100 µl | Horse |
Please visit cellsignal.com for individual component applications, species cross-reactivity, dilutions, protocols, and additional product information.
Description
The Cell Cycle/Checkpoint Antibody Sampler Kit provides a fast and economical means of evaluating multiple proteins involved in the cell cyle and checkpoint control. The kit contains enough primary and secondary antibody to perform four Western blot experiments.
Storage
Background
The cell division cycle demands accuracy to avoid the accumulation of genetic damage. This process is controlled by molecular circuits called "checkpoints" that are common to all eukaryotic cells (1). Checkpoints monitor DNA integrity and cell growth prior to replication and division at the G1/S and G2/M transitions, respectively. The cdc2-cyclin B kinase is pivotal in regulating the G2/M transition (2,3). Cdc2 is phosphorylated at Thr14 and Tyr15 during G2-phase by the kinases Wee1 and Myt1, rendering it inactive. The tumor suppressor protein retinoblastoma (Rb) controls progression through the late G1 restriction point (R) and is a major regulator of the G1/S transition (4). During early and mid G1-phase, Rb binds to and represses the transcription factor E2F (5). The phosphorylation of Rb late in G1-phase by CDKs induces Rb to dissociate from E2F, permitting the transcription of S-phase-promoting genes. In vitro, Rb can be phosphorylated at multiple sites by cdc2, cdk2, and cdk4/6 (6-8). DNA damage triggers both the G2/M and the G1/S checkpoints. DNA damage activates the DNA-PK/ATM/ATR kinases, which phosphorylate Chk at Ser345 (9), Chk2 at Thr68 (10) and p53 (11). The Chk kinases inactivate cdc25 via phosphorylation at Ser216, blocking the activation of cdc2.
- Nurse, P. (1997) Cell 91, 865-7.
- Norbury, C. and Nurse, P. (1992) Annu Rev Biochem 61, 441-70.
- Watanabe, N. et al. (1995) EMBO J 14, 1878-91.
- Sherr, C.J. (1996) Science 274, 1672-7.
- Dyson, N. (1998) Genes Dev 12, 2245-62.
- Kitagawa, M. et al. (1996) EMBO J 15, 7060-9.
- Lundberg, A.S. and Weinberg, R.A. (1998) Mol Cell Biol 18, 753-61.
- Harbour, J.W. et al. (1999) Cell 98, 859-69.
- Zhao, H. and Piwnica-Worms, H. (2001) Mol Cell Biol 21, 4129-39.
- Matsuoka, S. et al. (2000) Proc Natl Acad Sci USA 97, 10389-94.
- Tibbetts, R.S. et al. (1999) Genes Dev 13, 152-7.
Background References
Trademarks and Patents
Limited Uses
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