Phospho-FOXP3(S418) Antibody
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS: 3
- PROTOCOLS
- BACKGROUND
Application ![]()
| DB, E |
---|---|
Primary Accession | Q9BZS1 |
Other Accession | Q6U8D7, NP_054728 |
Reactivity | Human |
Predicted | Monkey |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 47244 Da |
Gene ID | 50943 |
---|---|
Other Names | Forkhead box protein P3, Scurfin, FOXP3, IPEX |
Target/Specificity | This FOXP3 Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S418 of human FOXP3. |
Dilution | DB~~1:500 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | Phospho-FOXP3(S418) Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | FOXP3 |
---|---|
Synonyms | IPEX |
Function | Transcriptional regulator which is crucial for the development and inhibitory function of regulatory T-cells (Treg) (PubMed:17377532, PubMed:21458306, PubMed:23947341, PubMed:24354325, PubMed:24722479, PubMed:24835996, PubMed:30513302, PubMed:32644293). Plays an essential role in maintaining homeostasis of the immune system by allowing the acquisition of full suppressive function and stability of the Treg lineage, and by directly modulating the expansion and function of conventional T-cells (PubMed:23169781). Can act either as a transcriptional repressor or a transcriptional activator depending on its interactions with other transcription factors, histone acetylases and deacetylases (PubMed:17377532, PubMed:21458306, PubMed:23947341, PubMed:24354325, PubMed:24722479). The suppressive activity of Treg involves the coordinate activation of many genes, including CTLA4 and TNFRSF18 by FOXP3 along with repression of genes encoding cytokines such as interleukin-2 (IL2) and interferon-gamma (IFNG) (PubMed:17377532, PubMed:21458306, PubMed:23947341, PubMed:24354325, PubMed:24722479). Inhibits cytokine production and T-cell effector function by repressing the activity of two key transcription factors, RELA and NFATC2 (PubMed:15790681). Mediates transcriptional repression of IL2 via its association with histone acetylase KAT5 and histone deacetylase HDAC7 (PubMed:17360565). Can activate the expression of TNFRSF18, IL2RA and CTLA4 and repress the expression of IL2 and IFNG via its association with transcription factor RUNX1 (PubMed:17377532). Inhibits the differentiation of IL17 producing helper T-cells (Th17) by antagonizing RORC function, leading to down-regulation of IL17 expression, favoring Treg development (PubMed:18368049). Inhibits the transcriptional activator activity of RORA (PubMed:18354202). Can repress the expression of IL2 and IFNG via its association with transcription factor IKZF4 (By similarity). |
Cellular Location | Nucleus {ECO:0000255|PROSITE-ProRule:PRU00089, ECO:0000269|PubMed:17360565, ECO:0000269|PubMed:18354202, ECO:0000269|PubMed:22678915, ECO:0000269|PubMed:23396208, ECO:0000269|PubMed:23973222, ECO:0000269|PubMed:23973223, ECO:0000269|PubMed:32644293}. Cytoplasm Note=Predominantly expressed in the cytoplasm in activated conventional T-cells whereas predominantly expressed in the nucleus in regulatory T- cells (Treg). The 41 kDa form derived by proteolytic processing is found exclusively in the chromatin fraction of activated Treg cells (By similarity). {ECO:0000250|UniProtKB:Q99JB6, ECO:0000269|PubMed:22678915} |

Provided below are standard protocols that you may find useful for product applications.
Background
The protein is a member of the forkhead/winged-helix family of transcriptional regulators. Defects in this gene are the cause of immunodeficiency polyendocrinopathy, enteropathy, X-linked syndrome (IPEX), also known as X-linked autoimmunity-immunodeficiency syndrome.
References
Davila, S., et al. Genes Immun. 11(3):232-238(2010)
Ganguly, S., et al. J. Invest. Dermatol. 130(4):1013-1022(2010)
Jung, D.J., et al. J. Biol. Chem. 285(11):7995-8002(2010)

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