Foxp3
Foxp3 (forkhead box P3, also known as scurfin, JM2, XPID, AIID, PIDX and DIETER) is a forkhead/winged-helix transcriptional regulator that is crucial for the development and inhibitory function of regulatory T-cells (Treg). Defects in the FOXP3 gene cause the X-linked IPEX syndrome. Browse Assay Genie's current range of Foxp3 research reagents below, or read on for the biology behind the target.
Foxp3 is a transcriptional regulator that is crucial for the development and inhibitory function of regulatory T-cells (Treg). It maintains immune homeostasis by allowing Treg to acquire full suppressive function and lineage stability, and by directly modulating the expansion and function of conventional T-cells. Foxp3 can act as either a transcriptional repressor or an activator, depending on its interactions with other transcription factors, histone acetylases and deacetylases.
Treg suppressive activity involves coordinated activation of genes including CTLA4 and TNFRSF18 by Foxp3, together with repression of cytokine genes such as interleukin-2 (IL2) and interferon-gamma (IFNG). Foxp3 inhibits cytokine production and T-cell effector function by repressing two key transcription factors, RELA and NFATC2. Repression of IL2 involves its association with the histone acetylase KAT5 and the histone deacetylase HDAC7. Through association with RUNX1, Foxp3 can activate TNFRSF18, IL2RA and CTLA4 while repressing IL2 and IFNG, and association with IKZF4 can also repress IL2 and IFNG. Foxp3 also inhibits differentiation of IL17-producing helper T-cells (Th17) by antagonising RORC, lowering IL17 expression and favouring Treg development, and it inhibits the transcriptional activator activity of RORA.
The protein is a member of the forkhead/winged-helix family of transcriptional regulators, and the Foxp3 gene belongs to the HGNC forkhead box group. UniProt lists its subcellular location as nucleus and cytoplasm, and alternatively spliced transcript variants encoding different isoforms have been identified. Defects in the gene cause immunodeficiency polyendocrinopathy, enteropathy, X-linked syndrome (IPEX), also known as X-linked autoimmunity-immunodeficiency syndrome, which is reflected in the IPEX and related aliases. A mouse ortholog, Foxp3, is recorded.
Foxp3 is crucial for the development, suppressive function and lineage stability of Treg, making it a central focus for studying immune homeostasis.
Foxp3 acts as repressor or activator through partners such as RUNX1, KAT5, HDAC7 and IKZF4, offering a model for cofactor-dependent gene control.
By antagonising RORC and reducing IL17 expression, Foxp3 favours Treg over Th17 development, relevant to studies of T-cell differentiation.
Defects in the Foxp3 gene cause IPEX syndrome, an X-linked autoimmune and immunodeficiency disorder studied in immune dysregulation research.
Foxp3 is a transcriptional regulator essential for the development and inhibitory function of regulatory T-cells. It represses genes such as IL2 and IFNG, activates CTLA4, TNFRSF18 and IL2RA, and restrains RELA, NFATC2 and RORC activity, helping maintain immune homeostasis.
Foxp3 is the forkhead box P3 gene product, also called scurfin, with aliases JM2, XPID, AIID, PIDX, DIETER and IPEX. The previous HGNC name was immune dysregulation, polyendocrinopathy, enteropathy, X-linked. Alternative splicing gives different isoforms, so check the datasheet of any product for its validated reactivity.
Defects in the Foxp3 gene cause IPEX syndrome, an X-linked immunodeficiency with polyendocrinopathy and enteropathy, also called X-linked autoimmunity-immunodeficiency syndrome. A mouse ortholog, Foxp3, exists, so the gene is studied in both species; check the datasheet of any product for its validated reactivity.
Other forkhead box proteins, Treg-associated genes and transcription factor partners of Foxp3 with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q9BZS1; product specifications from Assay Genie datasheets.