• Target：
• FoxO3A

• Fields：
• >>EGFR tyrosine kinase inhibitor resistance;>>Chemokine signaling pathway;>>FoxO signaling pathway;>>Mitophagy - animal;>>PI3K-Akt signaling pathway;>>AMPK signaling pathway;>>Longevity regulating pathway;>>Longevity regulating pathway - multiple species;>>Cellular senescence;>>Neurotrophin signaling pathway;>>Prolactin signaling pathway;>>Alcoholic liver disease;>>Shigellosis;>>Chemical carcinogenesis - reactive oxygen species;>>Endometrial cancer;>>Non-small cell lung cancer

• Gene Name：
• FOXO3

• Protein Name：
• Forkhead box protein O3

• Human Gene Id：
• 2309

• Human Swiss Prot No：
• O43524

• Mouse Gene Id：
• 56484

• Mouse Swiss Prot No：
• Q9WVH4

• Specificity：
• endogenous

• Formulation：
• PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA

• Source：
• Monoclonal, rabbit, IgG, Kappa

• Dilution：
• IHC 1:200-1:1000,WB 1:1000-1:5000,IF 1:200-1:1000,ELISA 1:5000-1:20000,IP 1:50-1:200,

• Purification：
• Protein A

• Storage Stability：
• -15°C to -25°C/1 year(Do not lower than -25°C)

• Other Name：
• FOXO3;FKHRL1;FOXO3A;Forkhead box protein O3;AF6q21 protein;Forkhead in rhabdomyosarcoma-like 1

• Molecular Weight(Da)：
• 71kD

• Observed Band(KD)：
• 97kD

• Background：
• This gene belongs to the forkhead family of transcription factors which are characterized by a distinct forkhead domain. This gene likely functions as a trigger for apoptosis through expression of genes necessary for cell death. Translocation of this gene with the MLL gene is associated with secondary acute leukemia. Alternatively spliced transcript variants encoding the same protein have been observed. [provided by RefSeq, Jul 2008],

• Function：
• disease:A chromosomal aberration involving FOXO3 is found in secondary acute leukemias. Translocation t(6;11)(q21;q23) with MLL/HRX.,function:Transcriptional activator which triggers apoptosis in the absence of survival factors, including neuronal cell death upon oxidative stress. Recognizes and binds to the DNA sequence 5'-[AG]TAAA[TC]A-3'.,PTM:In the presence of survival factors such as IGF-1, phosphorylated on Thr-32 and Ser-253 by AKT1/PKB. This phosphorylated form then interacts with 14-3-3 proteins and is retained in the cytoplasm. Survival factor withdrawal induces dephosphorylation and promotes translocation to the nucleus where the dephosphorylated protein induces transcription of target genes and triggers apoptosis. Although AKT1/PKB doesn't appear to phosphorylate Ser-315 directly, it may activate other kinases that trigger phosphorylation at this residue. Phosphorylated by ST

• Subcellular Location：
• Cytoplasm

• Expression：
• Ubiquitous.

Overexpression of HepaCAM inhibits bladder cancer cell proliferation and viability through the AKT/FoxO pathway. JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY J Cancer Res Clin. 2017 May;143(5):793-805 WB Human 1:1000 Bca cell

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