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Rabbit Anti-FOXP3 Polyclonal Antibody#abs131487

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Description

Catalog-specification	Delivery time	USD price
abs131487-50ug	In Stock	201.0
abs131487-100ug	In Stock	301.0

Overview
catalog	abs131487
Description	The immunodeficiency polyendocrinopathy, enteropathy, X-linked syndrome (IPEX), also known as X-linked autoimmunity-immunodeficiency syndrome, is caused by defects in FOXP3. This genetic condition leads to a range of symptoms including neonatal onset insulin-dependent diabetes mellitus, infections, secretory diarrhea, thrombocytopenia, anemia, and eczema. Unfortunately, IPEX is typically fatal during infancy.
Other names	AIID (Autoimmune enteropathy, Immunodeficiency and IPEX disorder) is a rare genetic condition characterized by immune dysregulation and polyendocrinopathy. It is caused by mutations in the FOXP3 gene, which codes for a protein called Forkhead box P3 (FOXP3). FOXP3 is vital for the development and function of regulatory T-cells, which play a crucial role in maintaining immune system balance. In individuals with AIID or IPEX, the FOXP3 gene is mutated, resulting in a dysfunctional FOXP3 protein. This leads to an overactive immune response and autoimmune disorders affecting multiple organs, particularly the intestines and endocrine glands. Symptoms of AIID and IPEX can include severe diarrhea, enteropathy (intestinal inflammation), eczema, type 1 diabetes, thyroid dysfunction, and other autoimmune diseases. The condition is more commonly seen in males due to its X-linked inheritance pattern. Diagnosis of AIID and IPEX is based on clinical symptoms, genetic testing, and analysis of FOXP3 protein expression or function. Early identification is essential for appropriate management and treatment options. Treatment for AIID and IPEX focuses on suppressing the abnormal immune response. This may involve immunosuppressive drugs, such as corticosteroids or calcineurin inhibitors, to reduce inflammation and prevent tissue damage. In severe cases, hematopoietic stem cell transplantation may be considered as a curative option. In conclusion, AIID and IPEX are rare genetic disorders associated with immune dysregulation and polyendocrinopathy. Understanding the role of FOXP3 gene and protein is crucial for diagnosis and management of these conditions. Ongoing research aims to develop better treatment strategies and improve the quality of life for individuals affected by AIID and IPEX.
Source	Rabbit
Specificity	The FOXP3 antibody has the ability to identify the complete levels of endogenous FOXP3. This means that it can detect all forms of FOXP3 present in a biological sample.
Species Reactivity	Human
Predictive reaction species	Pig;Sheep;Bovine;Horse;
Antigen	FOXP3
Application	Sure! Here's a rearranged version of the information provided: For western blotting (WB), dilutions of 1:500-1:2000 are recommended. Immunohistochemistry (IHC) should be performed using dilutions of 1:50-1:200. In the case of immunofluorescence (IF), a dilution range of 1:100-1:500 is suitable. For immunoprecipitation (IP), no specific dilution range is provided. For enzyme-linked immunosorbent assay (ELISA) using peptides, a dilution range of 1:20000-1:40000 is recommended.
Immunogen	A synthesized peptide derived from human FOXP3.
MW	47 kDa
Properties
Concentration	1mg/ml
purification	Utilizing SulfoLink™ Coupling Resin, peptide affinity chromatography was used to purify the antiserum. A highly similar content can be created by rearranging the phrasing while maintaining the original information: The process of purifying the antiserum involved peptide affinity chromatography, with SulfoLink™ Coupling Resin being employed.
Clonality	Polyclonal Antibody
Stability & Storage	Store at -20 °C for one year. Avoid repeated freeze/thaw cycles
Storage buffer	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.
Target
Background	Transcriptional regulator which is crucial for the development and inhibitory function of regulatory T-cells (Treg). 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. Can act either as a transcriptional repressor or a transcriptional activator depending on its interactions with other transcription factors, histone acetylases and deacetylases. 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). 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).
Tissue specificity	Down-regulated in regulatory T-cells (Treg) during inflammation.
Posttranslational modification	Polyubiquitinated, leading to its proteasomal degradation in regulatory T-cells (Treg) which is mediated by STUB1 in a HSPA1A/B-dependent manner. Deubiquitinated by USP7 leading to increase in protein stability.Phosphorylation at Ser-418 regulates its transcriptional repressor activity and consequently, regulatory T-cells (Treg) suppressive function. Dephosphorylated at Ser-418 by protein phosphatase 1 (PP1) in Treg cells derived from patients with rheumatoid arthritis. Phosphorylation by CDK2 negatively regulates its transcriptional activity and protein stability (By similarity).Acetylation on lysine residues stabilizes FOXP3 and promotes differentiation of T-cells into induced regulatory T-cells (iTregs) associated with suppressive functions. Deacetylated by SIRT1.Undergoes proteolytic cleavage in activated regulatory T-cells (Treg), and can be cleaved at either the N- or C-terminal site, or at both sites.
Celluar localization	Nucleus;
UniPort	Q9BZS1