Cell Signaling Technology

Product Pathways - PI3K / Akt Signaling

FoxO1 (L27) Antibody #9454

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Mk (C) Endogenous 78 to 82 Rabbit

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

Protocols

Specificity / Sensitivity

FoxO1 (L27) Antibody detects endogenous levels of total FoxO1 protein and does not cross-react with endogenous FoxO3a or FoxO4. The antibody also cross-reacts with an unidentified protein at 95 kDa.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to amino acids within the amino terminus of mouse FoxO1. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from IGROV-1 cells and untreated, λ phosphatase- or FBS-treated (20 min.) HeLa cells using FoxO1 (L27) Antibody.

Background

The Forkhead family of transcription factors is involved in tumorigenesis of rhabdomyosarcoma and acute leukemias (1-3). Within the family, three members (FoxO1, FoxO4, and FoxO3a) have sequence similarity to the nematode orthologue DAF-16, which mediates signaling via a pathway involving IGFR1, PI3K, and Akt (4-6). Active forkhead members act as tumor suppressors by promoting cell cycle arrest and apoptosis. Increased expression of any FoxO member results in the activation of the cell cycle inhibitor p27 Kip1. Forkhead transcription factors also play a part in TGF-β-mediated upregulation of p21 Cip1, a process negatively regulated through PI3K (7). Increased proliferation results when forkhead transcription factors are inactivated through phosphorylation by Akt at Thr24, Ser256, and Ser319, which results in nuclear export and inhibition of transcription factor activity (8). Forkhead transcription factors can also be inhibited by the deacetylase sirtuin (SirT1) (9).

  1. Anderson, M.J. et al. (1998) Genomics 47, 187-199.
  2. Galili, N. et al. (1993) Nat. Genet. 5, 230-235.
  3. Borkhardt, A. et al. (1997) Oncogene 14, 195-202.
  4. Nakae, J. et al. (1999) J. Biol. Chem. 274, 15982-15985.
  5. Rena, G. et al. (1999) J. Biol. Chem. 274, 17179-17183.
  6. Guo, S. et al. (1999) J. Biol. Chem. 274, 17184-17192.
  7. Seoane, J. et al. (2004) Cell 117, 211-223.
  8. Arden, K.C. (2004) Mol. Cell 14, 416-418.
  9. Yang, Y. et al. (2005) EMBO J. 24, 1021-1032.

Application References

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

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