R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
Phospho-FoxM1 (Thr600) (D9M6G) Rabbit mAb #14655
Filter:
- WB
- IP
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 125 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:200 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
Phospho-FoxM1 (Thr600) (D9M6G) Rabbit mAb recognizes endogenous levels of FoxM1 protein only when phosphorylated at Thr600.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr600 of human FoxM1 protein.
Background
Forkhead box M1 (FoxM1) is a forkhead box family transcription factor that regulates a number of genes throughout the cell cycle to help control DNA replication, mitosis, and cell proliferation. FoxM1 expression increases during G1 and S and reaches maximum levels in G2/M (1-3). Nuclear translocation occurs just before entry into G2/M and is associated with FoxM1 phosphorylation (4). Phosphorylation of FoxM1 by MAPK (Ser331, Ser704), Cyclin/Cdk (Ser4, Ser35, Thr600, Thr611, Thr620, Thr627, Ser638), Plk1 (Ser715, Ser724), and Chk2 (Ser376) stabilizes and activates FoxM1 (4-8). Forkhead box M1 is expressed in all embryonic tissues but is restricted to proliferating tissues in adults (9). Research studies show that FoxM1 expression is negatively regulated by p53 (10,11). Upregulation of FoxM1 is associated with many human cancers, including prostate, breast, lung, ovary, colon, pancreas, stomach, bladder, liver, and kidney, and may be associated with p53 mutations in some tumors (11,12). As a result, FoxM1 inhibitors have become a topic of interest for potential cancer therapy (13).
- Wang, I.C. et al. (2005) Mol Cell Biol 25, 10875-94.
- Leung, T.W. et al. (2001) FEBS Lett 507, 59-66.
- Wang, X. et al. (2002) Proc Natl Acad Sci U S A 99, 16881-6.
- Ma, R.Y. et al. (2005) J Cell Sci 118, 795-806.
- Laoukili, J. et al. (2008) Mol Cell Biol 28, 3076-87.
- Fu, Z. et al. (2008) Nat Cell Biol 10, 1076-82.
- Tan, Y. et al. (2007) Mol Cell Biol 27, 1007-16.
- Anders, L. et al. (2011) Cancer Cell 20, 620-34.
- Ye, H. et al. (1997) Mol Cell Biol 17, 1626-41.
- Barsotti, A.M. and Prives, C. (2009) Oncogene 28, 4295-305.
- Pandit, B. et al. (2009) Cell Cycle 8, 3425-7.
- Pilarsky, C. et al. (2004) Neoplasia 6, 744-50.
- Gartel, A.L. (2008) Expert Opin Ther Targets 12, 663-5.
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