Phospho-FoxO3a (Ser425) (D5E9T) Rabbit Antibody

INQUIRY

CAT. NO.: AMA-0414

Target Information
UniProt ID	O43524

Product Details
Size	100 µL
Reactivity	Human, Monkey
Host	Rabbit
Source/Isotype	Rabbit IgG
Storage	Store at -20°C. Do not aliquot the antibody.
Purification	Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser425 of human FoxO3a protein.

Usage
Application	WB, IP
Product Usage Information Dilution	Western Blotting (1:1000); Immunoprecipitation (1:50)
MW (Target)	82-97 kDa

Background
The Forkhead family of transcription factors is involved in tumorigenesis of rhabdomyosarcoma and acute leukemias 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 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 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 Forkhead transcription factors can also be inhibited by the deacetylase sirtuin (SirT1)ERK phosphorylates FoxO3a at Ser425, degrading FoxO3a via the ubiquitin-proteasome pathway. Research has shown that this phosphorylation event inhibits FoxO3a's function to induce cell death and thus promotes cell proliferation and tumorigenesis.

Background

The Forkhead family of transcription factors is involved in tumorigenesis of rhabdomyosarcoma and acute leukemias 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 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 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 Forkhead transcription factors can also be inhibited by the deacetylase sirtuin (SirT1)ERK phosphorylates FoxO3a at Ser425, degrading FoxO3a via the ubiquitin-proteasome pathway. Research has shown that this phosphorylation event inhibits FoxO3a's function to induce cell death and thus promotes cell proliferation and tumorigenesis.

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