antibody

Cdc20 (CDC20, Cdc20A, Cell Division Cycle 20, p55CDC, Fizzy)

C2559-01F

100 ul

polyclonal

domestic rabbit

nonconjugated

Cdc20 (CDC20, Cdc20A, Cell Division Cycle 20, p55CDC, Fizzy)

rabbit

Pab

Antibodies

100 ul

IgG

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 by cdks induces Rb to dissociate from E2F, permitting the transcription of S-phase-promoting genes. Rb can be phosphorylated at multiple sites in vitro 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. CDC20 binds to and activates the anaphase-promoting complex (APC) during mitosis and G1 phase of the cell cycle (12). Moreover, CDC20 is necessary for ubiquitin ligase activity of the APC/cyclosome (APC/C). In metaphase MAD2L1 inactivates the CDC20-APC/C complex, while in anaphase this inhibition is lost and CDC20-APC/C degrades its substrates (13). p53 and p21 suppress expression of CDC20 upon genotoxic stresses and ectopic introduction of p53. siRNA mediated knock-down of CDC20 in cancer cells leads to attenuated cell growth and induces G(2)/M arrest, suggesting that CDC20 is a possible therapeutic target of cancer (14). Organization of neuronal circuits requires presynaptic axonal differentiation and synapse formation. CDC20-APC regulates presynaptic differentiation in postmitotic neurons by triggering the required degradation of the transcription factor NeuroD2 (15). Applications: Suitable for use in Western Blot. Other applications not tested. Recommended Dilution: Western Blot: 1:1000. Incubate membrane with diluted antibody in 5% BSA, 1X TBS, 0.1% Tween-20 at 4°C with gentle shaking, overnight. Optimal dilutions to be determined by the researcher. Storage and Stability: May be stored at 4°C for short-term only. For long-term storage, aliquot and store at -20°C. Aliquots are stable for 12 months at -20°C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

Hu Mo Rt

Synthetic peptide corresponding to residues surrounding Ala35 of human CDC20.

Recognizes endogenous levels of total human CDC20. Species crossreactivity: mouse and rat.

Purified by Protein A and peptide affinity chromatography.

Supplied as a liquid in 10mM sodium HEPES, pH 7.5, 150mM sodium chloride, 0.1mg/ml BSA, 50% glycerol.

Not determined

Product Type: Pab Isotype: IgG Host: rabbit Source: human Concentration: Not determined Form: Supplied as a liquid in 10mM sodium HEPES, pH 7.5, 150mM sodium chloride, 0.1mg/ml BSA, 50% glycerol. Purity: Purified by Protein A and peptide affinity chromatography. Immunogen: Synthetic peptide corresponding to residues surrounding Ala35 of human CDC20. Specificity: Recognizes endogenous levels of total human CDC20. Species crossreactivity: mouse and rat. Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.

WB

-20°C

1. Nurse, P. (1997) Cell 91, 865-7, 2. Norbury, C. and Nurse, P. (1992) Annu Rev Biochem 61, 441-70, 3. Watanabe, N. et al. (1995) EMBO J. 14, 1878-1891, 4. Sherr, C.J. (1996) Science 274, 1672-1677, 5. Dyson, N. (1998) Genes Dev. 12, 2245-2262, 6. Kitagawa, M. et al. (1996) EMBO J. 15, 7060-7069, 7. Lundberg, A.S. and Weinberg, R.A. (1998) Mol Cell Biol 18, 753-761, 8. Harbour, J.W. et al. (1999) Cell 98, 859-869, 9. Zhao, H. and Piwnica-Worms, H. (2001) Mol. Cell Biol. 21, 4129-4139, 10. Matsuoka, S. et al. (2000) Proc. Natl. Acad. Sci. USA 97, 10389-10394, 11. Tibbetts, R.S. et al. (1999) Genes Dev. 13, 152-157, 12. Fang, G. et al. (1998) Mol Cell 2, 163-71, 13. Fang, G. et al. (1998) Genes Dev 12, 1871-83, 14. Kidokoro, T. et al. (2008) Oncogene 27, 1562-71, 15. Yang, Y. et al. (2009) Science 326, 575-8.

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