Product nameAnti-FOXO1A antibody [EP927Y] (Alexa Fluor® 488)
See all FOXO1A primary antibodies
DescriptionRabbit monoclonal [EP927Y] to FOXO1A (Alexa Fluor® 488)
ConjugationAlexa Fluor® 488. Ex: 495nm, Em: 519nm
Tested applicationsSuitable for: ICC/IF, Flow Cytmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
Synthetic peptide within Human FOXO1A. The exact sequence is proprietary. A synthetic peptide corresponding to residues surrounding Ser329 of human FOXO1A.
- ICC/IF: HeLa cells. Flow Cyt: HeLa cells.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents.
Alexa Fluor® is a registered trademark of Molecular Probes, Inc, a Thermo Fisher Scientific Company. The Alexa Fluor® dye included in this product is provided under an intellectual property license from Life Technologies Corporation. As this product contains the Alexa Fluor® dye, the purchase of this product conveys to the buyer the non-transferable right to use the purchased product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). As this product contains the Alexa Fluor® dye the sale of this product is expressly conditioned on the buyer not using the product or its components, or any materials made using the product or its components, in any activity to generate revenue, which may include, but is not limited to use of the product or its components: in manufacturing; (ii) to provide a service, information, or data in return for payment (iii) for therapeutic, diagnostic or prophylactic purposes; or (iv) for resale, regardless of whether they are sold for use in research. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, 5781 Van Allen Way, Carlsbad, CA 92008 USA or email@example.com.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Stable for 12 months at -20°C. Store In the Dark.
Storage bufferpH: 7.4
Preservative: 0.02% Sodium azide
Constituents: PBS, 30% Glycerol, 1% BSA
Concentration information loading...
PurityProtein A purified
- Signal Transduction
- Signaling Pathway
- Nuclear Signaling
- Nuclear Hormone Receptors
- Epigenetics and Nuclear Signaling
- Nuclear Signaling Pathways
- Nuclear Receptors
- Anti-FOXO1A antibody [EP927Y] (Alexa Fluor® 647) (ab200695)
- Anti-FOXO1A antibody [EP927Y] (Alexa Fluor® 594) (ab207242)
- Anti-FOXO1A antibody [EP927Y] (Alexa Fluor® 555) (ab207244)
- Anti-FOXO1A antibody [EP927Y] (Alexa Fluor® 568) (ab207245)
- Anti-FOXO1A antibody [EP927Y] - BSA and Azide free (ab219734)
- Anti-FOXO1A antibody [EP927Y] (ab52857)
Our Abpromise guarantee covers the use of ab200694 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
FunctionTranscription factor which acts as a regulator of cell responses to oxidative stress. In the presence of KIRT1, mediates down-regulation of cyclin D1 and up-regulation of CDKN1B levels which are required for cell transition from proliferative growth to quiescence.
Involvement in diseaseDefects in FOXO1 are a cause of rhabdomyosarcoma type 2 (RMS2) [MIM:268220]. It is a form of rhabdomyosarcoma, a highly malignant tumor of striated muscle derived from primitive mesenchimal cells and exhibiting differentiation along rhabdomyoblastic lines. Rhabdomyosarcoma is one of the most frequently occurring soft tissue sarcomas and the most common in children. It occurs in four forms: alveolar, pleomorphic, embryonal and botryoidal rhabdomyosarcomas. Note=Chromosomal aberrations involving FOXO1 are found in rhabdomyosarcoma. Translocation (2;13)(q35;q14) with PAX3; translocation t(1;13)(p36;q14) with PAX7. The resulting protein is a transcriptional activator.
Sequence similaritiesContains 1 fork-head DNA-binding domain.
modificationsPhosphorylated by AKT1; insulin-induced (By similarity). IGF1 rapidly induces phosphorylation of Ser-256, Thr-24, and Ser-319. 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 CK1, leading to nuclear exclusion and loss of function. Phosphorylation of Ser-329 is independent of IGF1 and leads to reduced function. Phosphorylated upon DNA damage, probably by ATM or ATR.
Cellular localizationCytoplasm. Nucleus. Shuttles between cytoplasm and nucleus.
- Information by UniProt
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Overlay histogram showing HeLa cells stained with ab200694 (red line). The cells were fixed with 4% formaldehyde (10 min) and then permeabilized with 0.1% PBS-Tween for 20 min. The cells were then incubated in 1x PBS / 10% normal goat serum / 0.3M glycine to block non-specific protein-protein interactions followed by the antibody (ab200694, 1/50 dilution) for 30 min at 22°C. Isotype control antibody (black line) was rabbit monoclonal IgG [EPR25A] Alexa Fluor® 488 (ab199091) used at the same concentration and conditions as the primary antibody. Unlabelled sample (blue line) was also used as a control. Acquisition of >5,000 events were collected using a 20mW Argon ion laser (488nm) and 525/30 bandpass filter. This antibody gave a positive signal in HeLa cells fixed with 80% methanol (5 min)/permeabilized with 0.1% PBS-Tween for 20 min used under the same conditions.
ab200694 staining FOXOA1 in HeLa cells. The cells were fixed with 4% formaldehyde (10min), permeabilized with 0.1% Triton X-100 for 5 minutes and then blocked with 1% BSA/10% normal goat serum/0.3M glycine in 0.1% PBS-Tween for 1h. The cells were then incubated overnight at +4°C with ab200694 at 1/200 dilution (shown in green) and ab195889, Mouse monoclonal to alpha Tubulin (Alexa Fluor® 594), at 2µg/ml (shown in red). Nuclear DNA was labelled with DAPI (shown in blue).
Image was taken with a confocal microscope (Leica-Microsystems, TCS SP8).
ab200694 has not yet been referenced specifically in any publications.