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Anti-FoxO3a Rabbit Antibody [L2E7]

Catalog No.: F4129

Application: Reactivity: Mouse, Rat, Human

Usage Information

Dilution
WB1:1000 IP1:50 IHC1:1600 - 1:6400 IF1:400 - 1:800 FCM1:200 - 1:800

Application
WB, IP, IHC, IF, FCM

Reactivity
Mouse, Rat, Human

Source
Rabbit

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
82-97 kDa

Datasheet & SDS

Biological Description

Specificity
Anti-FoxO3a Rabbit Antibody [L2E7] recognizes endogenous levels of total FoxO3a protein.

Clone
L2E7

Synonym(s)
Forkhead box protein O3, AF6q21 protein, Forkhead in rhabdomyosarcoma-like 1, FOXO3, FKHRL1, FOXO3A

Background
Forkhead box O (FoxO) transcription factors, the mammalian homologues of the C. elegans DAF-16 protein, share a conserved 110–amino acid forkhead box (winged-helix) DNA-binding domain. Among the mammalian FoxO family, the major members include FoxO1, FoxO3a, FoxO4, and FoxO6. FoxO3a acts primarily as a tumor suppressor by regulating genes involved in apoptosis, cell-cycle arrest, autophagy, and oxidative stress resistance. It can block cell-cycle progression, trigger programmed cell death, and enhance autophagy as a protective response to environmental stress, thereby contributing to cellular homeostasis. Dysregulation of FoxO3a has been implicated in various human diseases. At the transcriptional level, FoxO3a directly binds promoters of apoptotic genes (e.g., Bim, FasL, TRAIL), cell-cycle inhibitors (p27, p21), autophagy-related genes (Gabarapl1, ATG12), and stress response genes (MnSOD, catalase). FoxO3a activity is tightly controlled by post-translational modifications, including phosphorylation, acetylation, and ubiquitination. Among these, phosphorylation plays a central role. Protein kinase B (Akt) phosphorylates FoxO3a at Thr32, Ser253, and Ser315, with Ser253 being particularly important for regulating nuclear–cytoplasmic shuttling. Once phosphorylated, FoxO3a associates with the 14-3-3 protein, which masks its nuclear localization signals, driving its export from the nucleus and blocking re-entry. In addition, Akt-dependent phosphorylation promotes interaction with ubiquitin E3 ligases, leading to polyubiquitination and subsequent proteasomal degradation of FoxO3a. Thus, the Akt signaling pathway is a key regulator of FoxO3a stability and function, balancing its tumor-suppressive and stress-response roles.

Background

Forkhead box O (FoxO) transcription factors, the mammalian homologues of the C. elegans DAF-16 protein, share a conserved 110–amino acid forkhead box (winged-helix) DNA-binding domain. Among the mammalian FoxO family, the major members include FoxO1, FoxO3a, FoxO4, and FoxO6. FoxO3a acts primarily as a tumor suppressor by regulating genes involved in apoptosis, cell-cycle arrest, autophagy, and oxidative stress resistance. It can block cell-cycle progression, trigger programmed cell death, and enhance autophagy as a protective response to environmental stress, thereby contributing to cellular homeostasis. Dysregulation of FoxO3a has been implicated in various human diseases. At the transcriptional level, FoxO3a directly binds promoters of apoptotic genes (e.g., Bim, FasL, TRAIL), cell-cycle inhibitors (p27, p21), autophagy-related genes (Gabarapl1, ATG12), and stress response genes (MnSOD, catalase). FoxO3a activity is tightly controlled by post-translational modifications, including phosphorylation, acetylation, and ubiquitination. Among these, phosphorylation plays a central role. Protein kinase B (Akt) phosphorylates FoxO3a at Thr32, Ser253, and Ser315, with Ser253 being particularly important for regulating nuclear–cytoplasmic shuttling. Once phosphorylated, FoxO3a associates with the 14-3-3 protein, which masks its nuclear localization signals, driving its export from the nucleus and blocking re-entry. In addition, Akt-dependent phosphorylation promotes interaction with ubiquitin E3 ligases, leading to polyubiquitination and subsequent proteasomal degradation of FoxO3a. Thus, the Akt signaling pathway is a key regulator of FoxO3a stability and function, balancing its tumor-suppressive and stress-response roles.

References
https://pubmed.ncbi.nlm.nih.gov/25225602/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%