Monoclonal Antibody to FOXO1 (Clone: ABM4E66) FITC Conjugated
Fig-1: Intracellular FLOW analysis of THP1 cells using 0.5 µg of FITC conjugated Anti-FOXO1 antibody. Green represents Mouse IgG2b FITC isotype control. Red represents FITC conjugated Anti-FOXO1 (clone: ABM4E66) antibody.
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| Format : | Purified |
| Amount : | 100 µg |
| Isotype : | Mouse IgG2b Kappa |
| Purification : | Protein G Chromatography |
| Content : | 25 µg in 50 µl/100 µg in 200 µl Tris buffer containing 0.05% sodium azide. Sodium azide is highly toxic. |
| Storage condition : | Store the antibody at 4°C; stable for 6 months. |
FOXO1 is one of the fox proteins playing pivotal roles in several human intracellular pathways. These proteins are transcription factors acting as nuclear regulator of transcriptional activity of a number of metabolic processes such as the cellular response to oxidative stress. FOXO1 protein response to oxidative stress may be linked to Alzheimer's disease (AD) by means of insulin brain resistance. FOXO1 plays a critical role in establishing and maintaining the B cell specific differentiation program, but it is also responsible for cell death due to an inappropriate BCR signaling. This protein is highly expressed in B cells, is downregulated in Hodgkin and Reed-Sternberg (HRS) cells of cHL (Classical Hodgkin Lymphoma).
FACS : 0.5 µg/ 10^6 cells
For Research Use Only. Not for use in diagnostic/therapeutics procedures.
| Subcellular location: | Cytoplasm, Nucleus |
| Post transnational modification: | 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. |
| Tissue Specificity: | Ubiquitous. |
| BioGrid: | 108597. 63 interactions. |
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