Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

FoxM1 Antibody #3948

Applications Reactivity Sensitivity MW (kDa) Source
W H M Endogenous 110 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

FoxM1 Antibody detects endogenous levels of total FoxM1 protein. All three alternative splice variants are predicted to be recognized (FoxM1a, FoxM1b, and FoxM1c).

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human FoxM1 protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from COS cells, mock transfected (-) or transfected with FoxM1 (+), using FoxM1 Antibody.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa cells, synchronized in S phase by double thymidine block followed by release for the indicated times, using FoxM1 Antibody.

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 (Thr600, Thr611, Thr672), Plk1 (Ser715, Ser724), and Chk2 (Ser376) stabilizes and activates FoxM1 (4-7). Forkhead box M1 is expressed in all embryonic tissues but is restricted to proliferating tissues in adults (8). Recent studies have shown that FoxM1 expression is negatively regulated by p53 (9,10). 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 (10,11). As a result, FoxM1 inhibitors have become a topic of interest for potential cancer therapy (12).

  1. Wang, I.C. et al. (2005) Mol Cell Biol 25, 10875-94.
  2. Leung, T.W. et al. (2001) FEBS Lett 507, 59-66.
  3. Wang, X. et al. (2002) Proc Natl Acad Sci USA 99, 16881-6.
  4. Ma, R.Y. et al. (2005) J Cell Sci 118, 795-806.
  5. Laoukili, J. et al. (2008) Mol Cell Biol 28, 3076-87.
  6. Fu, Z. et al. (2008) Nat Cell Biol 10, 1076-82.
  7. Tan, Y. et al. (2007) Mol Cell Biol 27, 1007-16.
  8. Ye, H. et al. (1997) Mol Cell Biol 17, 1626-41.
  9. Barsotti, A.M. and Prives, C. (2009) Oncogene 28, 4295-305.
  10. Pandit, B. et al. (2009) Cell Cycle 8, 3425-7.
  11. Pilarsky, C. et al. (2004) Neoplasia 6, 744-50.
  12. Gartel, A.L. (2008) Expert Opin Ther Targets 12, 663-5.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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