FoxO1 Antibody (YA5121)
(Synonyms: FOXO1; FKHR; FOXO1A; Forkhead box protein O1; Forkhead box protein O1A; Forkhead in rhabdomyosarcoma)FoxO1 Antibody (YA5121) is a Mouse-derived and non-conjugated monoclonal antibody, targeting to FoxO1.
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Host:
Mouse
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Application:
WB, ICC/IF
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Reactivity :
Human, Mouse
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Formulation:
Supplied in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
|---|---|---|
| Dilution Ratio | 1:1000-1:2000 | 1:100-1:500 |
Product Details
FoxO1 Antibody (YA5121) is a Mouse-derived and non-conjugated monoclonal antibody, targeting to FoxO1.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Mouse
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Calculated Molecular Weight Predicted band size: 70 kDa;
Purified recombinant human FoxO1A (C-terminus) protein fragments expressed in E.coli.
affinity purified.
Non-conjugated
Unmodified
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
FOXO1 is a Forkhead box O transcription factor regulated by insulin/PI3K/Akt signaling, and it coordinates gene programs controlling metabolism, apoptosis, cell-cycle arrest, oxidative-stress resistance, and DNA repair[1]. Mechanistically, insulin or growth-factor stimulation phosphorylates FOXO proteins through Akt, drives nuclear export, and suppresses FOXO-dependent transcription[1]. In ovarian granulosa cells, FSH and IGF-1 activate PI3K/AKT signaling downstream through FOXO1, supporting gene expression linked to follicle maturation[2]. In diabetes models, FOXO1 regulates hepatic glucose production, and selective FOXO1 inhibition improved insulin sensitivity and glucose control in db/db mice without weight gain[3]. Compared with related isoforms, mammals contain FOXO1, FOXO3, FOXO4, and FOXO6, but FoxO1- mice die at embryonic day 10.5 from angiogenesis defects, while FoxO3- and FoxO4- mice are viable[1]. This isoform distinction supports FOXO1-focused experimental designs when metabolic control, hepatic glucose output, or developmental vascular phenotypes are primary endpoints[1][3]. For experimental applications, compound 10 showed higher FOXO1 selectivity than AS1842856 and served as a superior tool molecule for investigating FOXO1 function in vitro and in vivo[3].
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Subcellular Localization
Cytoplasm; Nucleus
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Expression
Tissue_specificity:It is expressed in umbilical cord endothelial cells (protein level) (PubMed: 19483080) . It is highly expressed in skeletal muscle and ovaries, and less so in the heart, placenta, lungs, liver, pancreas, spleen, testes, and small intestine (PubMed: 9479491) . It is weakly expressed in the brain, thymus, prostate, and colonic mucosa (PubMed: 9479491) .
Induction:Expression is regulated by KRIT1. Levels of expression also regulated by FOXC1 which binds to a conserved element in the FOXO1 promoter -
Subunit
Interacts with LRPPRC. Interacts with RUNX2; the interaction inhibits RUNX2 transcriptional activity and mediates the IGF1/insulin-dependent BGLAP expression in osteoblasts Interacts with PPP2R1A; the interaction regulates the dephosphorylation of FOXO1 at Thr-24 and Ser-256 leading to its nuclear import. Interacts (acetylated form) with PPARG. Interacts with XBP1 isoform 2; this interaction is direct and leads to FOXO1 ubiquitination and degradation via the proteasome pathway (By similarity). Interacts with NLK. Interacts with SIRT1; the interaction results in the deacetylation of FOXO1 leading to activation of FOXO1-mediated transcription of genes involved in DNA repair and stress resistance. Binds to CDK1. Interacts with the 14-3-3 proteins, YWHAG and YWHAZ; the interactions require insulin-stimulated phosphorylation on Thr-24, promote nuclear exit and loss of transcriptional activity. Interacts with SKP2; the interaction ubiquitinates FOXO1 leading to its proteasomal degradation. The interaction requires the presence of KRIT1. Interacts (via the C-terminal half) with ATF4 (via its DNA-binding domain); the interaction occurs in osteoblasts, regulates glucose homeostasis via suppression of beta-cell proliferation and subsequent decrease in insulin production. Interacts with PRMT1; the interaction methylates FOXO1, prevents PKB/AKT1 phosphorylation and retains FOXO1 in the nucleus. Interacts with EP300 and CREBBP; the interactions acetylate FOXO1. Interacts with SIRT2; the interaction is disrupted in response to oxidative stress or serum deprivation, leading to increased level of acetylated FOXO1, which promotes stress-induced autophagy by stimulating E1-like activating enzyme ATG7. Interacts (acetylated form) with ATG7; the interaction is increased in response to oxidative stress or serum deprivation and promotes the autophagic process leading to cell death. Interacts (via the Fork-head domain) with CEBPA; the interaction increases when FOXO1 is deacetylated. Interacts with WDFY2. Forms a complex with WDFY2 and AKT1 (By similarity). Interacts with CRY1 (By similarity). Interacts with PPIA/CYPA; the interaction promotes FOXO1 dephosphorylation, nuclear accumulation and transcriptional activity (PubMed:31063815). Interacts with TOX4; FOXO1 is required for full induction of TOX4-dependent activity and the interaction is inhibited by insulin (By similarity). Interacts (when phosphorylated on Ser-256) with STUB1/CHIP (PubMed:19483080)
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SwissProt ID
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Synonyms
FOXO1; FKHR; FOXO1A; Forkhead box protein O1; Forkhead box protein O1A; Forkhead in rhabdomyosarcoma
Documentation
[1]. Carter ME, et al. FOXO transcription factors. Curr Biol. 2007 Feb 20;17(4):R113-4. [Content Brief]
[2]. Law NC, et al. Insulin Receptor Substrate 1, the Hub Linking Follicle-stimulating Hormone to Phosphatidylinositol 3-Kinase Activation. J Biol Chem. 2016 Feb 26;291(9):4547-60. [Content Brief]
[3]. Lee YK, et al. FOXO1 inhibition synergizes with FGF21 to normalize glucose control in diabetic mice. Mol Metab. 2021 Jul;49:101187. [Content Brief]
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