Product: Acetyl-FOXO1A (Lys294) Antibody
Catalog: AF2305
Description: Rabbit polyclonal antibody to Acetyl-FOXO1A (Lys294)
Application: WB IHC
Cited expt.: WB, IHC
Reactivity: Human, Mouse, Rat, Monkey
Prediction: Pig, Bovine, Dog, Chicken, Xenopus
Mol.Wt.: 70kDa,90kDa; 70kD(Calculated).
Uniprot: Q12778
RRID: AB_2845319

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat,Monkey
Prediction:
Pig(100%), Bovine(100%), Dog(100%), Chicken(100%), Xenopus(91%)
Clonality:
Polyclonal
Specificity:
Acetyl-FOXO1A (Lys294) Antibody detects endogenous levels of Acetyl-FOXO1A only when acetylated at Lys294.
RRID:
AB_2845319
Cite Format: Affinity Biosciences Cat# AF2305, RRID:AB_2845319.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

FKH 1; FKH1; FKHR; Forkhead (Drosophila) homolog 1 (rhabdomyosarcoma); Forkhead box O1; Forkhead box protein O1; Forkhead box protein O1A; Forkhead in rhabdomyosarcoma; Forkhead, Drosophila, homolog of, in rhabdomyosarcoma; FoxO transcription factor; foxo1; FOXO1_HUMAN; FOXO1A; OTTHUMP00000018301;

Immunogens

Immunogen:

A synthesized peptide derived from human FOXO1A around the acetylation site of Lys294.

Uniprot:
Gene(ID):
Expression:
Q12778 FOXO1_HUMAN:

Ubiquitous.

Sequence:
MAEAPQVVEIDPDFEPLPRPRSCTWPLPRPEFSQSNSATSSPAPSGSAAANPDAAAGLPSASAAAVSADFMSNLSLLEESEDFPQAPGSVAAAVAAAAAAAATGGLCGDFQGPEAGCLHPAPPQPPPPGPLSQHPPVPPAAAGPLAGQPRKSSSSRRNAWGNLSYADLITKAIESSAEKRLTLSQIYEWMVKSVPYFKDKGDSNSSAGWKNSIRHNLSLHSKFIRVQNEGTGKSSWWMLNPEGGKSGKSPRRRAASMDNNSKFAKSRSRAAKKKASLQSGQEGAGDSPGSQFSKWPASPGSHSNDDFDNWSTFRPRTSSNASTISGRLSPIMTEQDDLGEGDVHSMVYPPSAAKMASTLPSLSEISNPENMENLLDNLNLLSSPTSLTVSTQSSPGTMMQQTPCYSFAPPNTSLNSPSPNYQKYTYGQSSMSPLPQMPIQTLQDNKSSYGGMSQYNCAPGLLKELLTSDSPPHNDIMTPVDPGVAQPNSRVLGQNVMMGPNSVMSTYGSQASHNKMMNPSSHTHPGHAQQTSAVNGRPLPHTVSTMPHTSGMNRLTQVKTPVQVPLPHPMQMSALGGYSSVSSCNGYGRMGLLHQEKLPSDLDGMFIERLDCDMESIIRNDLMDGDTLDFNFDNVLPNQSFPHSVKTTTHSWVSG

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Bovine
100
Dog
100
Chicken
100
Xenopus
91
Horse
0
Sheep
0
Zebrafish
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

Research Backgrounds

Function:

Transcription factor that is the main target of insulin signaling and regulates metabolic homeostasis in response to oxidative stress. Binds to the insulin response element (IRE) with consensus sequence 5'-TT[G/A]TTTTG-3' and the related Daf-16 family binding element (DBE) with consensus sequence 5'-TT[G/A]TTTAC-3'. Activity suppressed by insulin. Main regulator of redox balance and osteoblast numbers and controls bone mass. Orchestrates the endocrine function of the skeleton in regulating glucose metabolism. Acts synergistically with ATF4 to suppress osteocalcin/BGLAP activity, increasing glucose levels and triggering glucose intolerance and insulin insensitivity. Also suppresses the transcriptional activity of RUNX2, an upstream activator of osteocalcin/BGLAP. In hepatocytes, promotes gluconeogenesis by acting together with PPARGC1A and CEBPA to activate the expression of genes such as IGFBP1, G6PC and PCK1. Important regulator of cell death acting downstream of CDK1, PKB/AKT1 and STK4/MST1. Promotes neural cell death. Mediates insulin action on adipose tissue. Regulates the expression of adipogenic genes such as PPARG during preadipocyte differentiation and, adipocyte size and adipose tissue-specific gene expression in response to excessive calorie intake. Regulates the transcriptional activity of GADD45A and repair of nitric oxide-damaged DNA in beta-cells. Required for the autophagic cell death induction in response to starvation or oxidative stress in a transcription-independent manner. Mediates the function of MLIP in cardiomyocytes hypertrophy and cardiac remodeling (By similarity).

PTMs:

Phosphorylation by NLK promotes nuclear export and inhibits the transcriptional activity. In response to growth factors, phosphorylation on Thr-24, Ser-256 and Ser-322 by PKB/AKT1 promotes nuclear export and inactivation of transactivational activity. Phosphorylation on Thr-24 is required for binding 14-3-3 proteins. Phosphorylation of Ser-256 decreases DNA-binding activity and promotes the phosphorylation of Thr-24 and Ser-319, permitting phosphorylation of Ser-322 and Ser-325, probably by CDK1, leading to nuclear exclusion and loss of function. Stress signals, such as response to oxygen or nitric oxide, attenuate the PKB/AKT1-mediated phosphorylation leading to nuclear retention. Phosphorylation of Ser-329 is independent of IGF1 and leads to reduced function. Dephosphorylated on Thr-24 and Ser-256 by PP2A in beta-cells under oxidative stress leading to nuclear retention (By similarity). Phosphorylation of Ser-249 by CDK1 disrupts binding of 14-3-3 proteins leading to nuclear accumulation and has no effect on DNA-binding nor transcriptional activity. Phosphorylation by STK4/MST1 on Ser-212, upon oxidative stress, inhibits binding to 14-3-3 proteins and nuclear export.

Acetylated. Acetylation at Lys-262, Lys-265 and Lys-274 are necessary for autophagic cell death induction. Deacetylated by SIRT2 in response to oxidative stress or serum deprivation, thereby negatively regulating FOXO1-mediated autophagic cell death.

Ubiquitinated by SKP2. Ubiquitination leads to proteasomal degradation.

Methylation inhibits AKT1-mediated phosphorylation at Ser-256 and is increased by oxidative stress.

Once in the nucleus, acetylated by CREBBP/EP300. Acetylation diminishes the interaction with target DNA and attenuates the transcriptional activity. It increases the phosphorylation at Ser-256. Deacetylation by SIRT1 results in reactivation of the transcriptional activity. Oxidative stress by hydrogen peroxide treatment appears to promote deacetylation and uncoupling of insulin-induced phosphorylation. By contrast, resveratrol acts independently of acetylation.

Subcellular Location:

Cytoplasm. Nucleus.
Note: Shuttles between the cytoplasm and nucleus. Largely nuclear in unstimulated cells. In osteoblasts, colocalizes with ATF4 and RUNX2 in the nucleus (By similarity). Insulin-induced phosphorylation at Ser-256 by PKB/AKT1 leads, via stimulation of Thr-24 phosphorylation, to binding of 14-3-3 proteins and nuclear export to the cytoplasm where it is degraded by the ubiquitin-proteosomal pathway. Phosphorylation at Ser-249 by CDK1 disrupts binding of 14-3-3 proteins and promotes nuclear accumulation. Phosphorylation by NLK results in nuclear export. Translocates to the nucleus upon oxidative stress-induced phosphorylation at Ser-212 by STK4/MST1. SGK1-mediated phosphorylation also results in nuclear translocation. Retained in the nucleus under stress stimuli including oxidative stress, nutrient deprivation or nitric oxide. Retained in the nucleus on methylation.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Ubiquitous.

Research Fields

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Environmental Information Processing > Signal transduction > FoxO signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > AMPK signaling pathway.   (View pathway)

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.

· Human Diseases > Cancers: Specific types > Prostate cancer.   (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway.   (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway - multiple species.   (View pathway)

· Organismal Systems > Endocrine system > Insulin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Thyroid hormone signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Glucagon signaling pathway.

References

1). Circular RNA FEACR inhibits ferroptosis and alleviates myocardial ischemia/reperfusion injury by interacting with NAMPT. Journal of biomedical science, 2023 (PubMed: 37370086) [IF=9.0]

2). ATP-citrate lyase controls endothelial gluco-lipogenic metabolism and vascular inflammation in sepsis-associated organ injury. Cell death & disease, 2023 (PubMed: 37414769) [IF=8.1]

Application: WB    Species: human    Sample: HUVEC

Fig. 5: ACLY regulated MYC expression via promoting the acetylation of FoxO1 and H3. A KEGG analysis of DEGs from transcriptomic sequencing showing the top 20 enriched pathways involved in ACLY regulation in LPS-induced HUVEC. B, C Levels of acetyl-CoA in HUVEC treated with BMS-303141 before LPS stimulation were measured (n = 6). D Western blot analysis showing the global acetylation of lysine in HUVEC treated with or without BMS-303141 before LPS stimulation. (E–H) HUVEC were pretreated with BMS-303141 or transfected with siRNA specific to ACLY before stimulatedn with LPS for 1 h. Levels of phosphorylated and total ACLY, acetylated and total FoxO1, as well as MYC were tested using Western blot assays. I Immunofluorescence staining showing FoxO1 localization in HUVEC stimulated with LPS in the presence of BMS-303141 (10 µM) or C646 (5 µM). J, K Western blot analysis showing the levels of acetylated FoxO1 and acetylated H3, and the expression of MYC in HUVEC with ACLY-WT (WT) or ACLY-S455D (S455D) overexpression, respectively. L Immunofluorescence staining representing FoxO1 nuclear export in ACLY-WT- and ACLY-S455D-overexpressing HUVEC (white arrow). M, N ACLY-WT-overexpressing (WT) or ACLY-S455D-overexpressing (S455D) HUVEC were treated with p300 inhibitor C646 (5 µM) and the levels of

3). S100A11 Promotes Liver Steatosis via FOXO1-Mediated Autophagy and Lipogenesis. Cellular and Molecular Gastroenterology and Hepatology, 2021 (PubMed: 33075563) [IF=7.1]

Application: WB    Species: mouse    Sample: Hepa 1–6 cells

Figure 16. |(See previous page). Inhibition of FOXO1 and autophagy decreased lipid content and the level of proteins related to the autophagy process in the S100A11 overexpression Hepa 1–6 cells.(F) Quantification of the results from panel E by ImageJ. Western blot detection and quantification of related proteins in the S100A11 overexpression Hepa 1–6 cells treated with (G and H) 10 nmol/L BAF, (I and J) 2 mmol/L 3-MA, and (K and L) RNA interference of Atg7, respectively.

4). Autophagy promotes directed migration of HUVEC in response to electric fields through the ROS/SIRT1/FOXO1 pathway. Free Radical Biology and Medicine, 2022 (PubMed: 36162742) [IF=7.1]

5). Puerarin suppresses macrophage M1 polarization to alleviate renal inflammatory injury through antagonizing TLR4/MyD88-mediated NF-κB p65 and JNK/FoxO1 activation. Phytomedicine : international journal of phytotherapy and phytopharmacology, 2024 (PubMed: 38905846) [IF=6.7]

6). Leucine Supplementation in Middle-Aged Male Mice Improved Aging-Induced Vascular Remodeling and Dysfunction via Activating the Sirt1-Foxo1 Axis. Nutrients, 2022 (PubMed: 36145233) [IF=5.9]

7). Ginsenoside Rc Alleviates Myocardial Ischemia-Reperfusion Injury by Reducing Mitochondrial Oxidative Stress and Apoptosis: Role of SIRT1 Activation. Journal of Agricultural and Food Chemistry, 2023 (PubMed: 36626267) [IF=5.7]

8). Fraxetin attenuates DNA damage and inflammation in cisplatin-induced nephrotoxicity via FoxO1 activation. International immunopharmacology, 2025 (PubMed: 39765000) [IF=5.6]

9). Paternal High-Fat Diet Altered Sperm 5'tsRNA-Gly-GCC Is Associated With Enhanced Gluconeogenesis in the Offspring. Frontiers in Molecular Biosciences, 2022 (PubMed: 35480893) [IF=5.0]

10). NAD-Dependent Protein Deacetylase Sirtuin-1 Mediated Mitophagy Regulates Early Brain Injury After Subarachnoid Hemorrhage. Journal of inflammation research, 2024 (PubMed: 38562659) [IF=4.5]

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