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Validated All-in-One™ qPCR Primer for FOXP3(NM_014009.3) Search again
Product ID:
HQP012269
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AIID, DIETER, IPEX, JM2, PIDX, XPID
Gene Description:
forkhead box P3
Target Gene Accession:
NM_014009.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The protein encoded by this gene 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. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq].
Gene References into function
- The ability of scurfin to bind DNA, and presumably repress transcription, plays a paramount role in determining the amplitude of the response of CD4 T cells to activation.
- novel mutations of FOXP3 in two Japanese patients with immune dysregulation, polyendocrinopathy, enteropathy, X linked syndrome (IPEX)
- Random X inactivation was found in the T lymphocytes of a carrier of a FOXP3 mutation (Ala384Thr)with an affected son.
- FoxP3 is expressed predominantly in Tr cells and that it may serve as a master regulator of this cell population.
- characterization of the underlying FOXP3 mutation in two families with features consistent with IPEX; analysis elucidated the molecular basis of IPEX in one family and provided evidence for an autosomal locus, suggesting genetic heterogeneity
- impact of disease-causing missense mutations on the three-dimensional structure, stability, and surface electrostatic charge distribution of the forkhead domains is examined
- TGF-beta-mediated induction of Foxp3 in CD4+CD25- T cells results in the development of T cells with regulatory functions.
- Foxp3 regulatory gene expression may have a role in graft-versus-host disease
- Allelic variation in or near the coding regions of the FOXP3 gene does not have a major role in the inherited susceptibility to the common form of type 1 diabetes.
- Human cord blood CD25+CD4+ T cells preferentially transcribed Foxp3, which governs the regulatory function of this subset i
- FoxP3 protein, but not mRNA, was specifically expressed by cord blood CD4-CD25 derived T-cells
- FOXP3 is a crucial regulatory gene for the development and function of CD25(+)CD4(+) regulatory T cells
- FOXP3 expression in humans, unlike mice, may not be specific for cells with a regulatory phenotype and may be only a consequence of activation status.
- The relative expression of FOXP3 protein mrNA was estimated by the ratio of the Foxp3 value to the HPRT value.
- Multiple sclerosis patients have abnormalities in FOXP3 message and protein expression levels in peripheral CD4+ CD25+ T cells that are quantitatively related to a reduction in functional suppression induced during suboptimal T-cell receptor ligation.
- Gene expression of regulatory T cells transcription factor FOXP3 was reduced in chronic graft-versus-host disease patients
- FOXP3 mRNA expression levels in allostimulated CD25 cells and CD25 cells and in peripheral blood mononuclear cells.
- Initiation and suppressive function of FOXP3 and regulatory T cells in the context of allergic asthma. Review.
- Ectopic expression of FOXP3 in human CD4+ T cells does not act as a molecular switch to induce regulatory T cells in vitro
- The determination of FOXP3+/CD8+ ratio can be a helpful tool to discriminate graft versus hosst disease from infectious inflammation after allogeneic stem cell transplantation.
- High expression levels of FoxP3 is associated with ovarian cancer
- Costimulation of effector T cells with anti-CD3 and TLR5 ligand flagellin resulted in enhanced proliferation and production of IL-2, and potently increased their suppressive capacity and enhanced expression of FOXP3.
- Increased expression of interleukin-10 and transforming growth factor-beta1 mRNA was also detected in patients with TB but did not correlate with regulatory T-cell markers.
- analysis of transcriptional regulation by FOXP3 [review]
- Increase of functional FOXP3 in T cells in cancer patients is a response to the process of malignant transformation.
- Fox3p expression is inherent feature of the function of type 1 regulatory T cells specific for desmoglein-3, the autoantigen of pemphigus vulgaris.
- reveals the structure of the human FOXP3 promoter and provides new insights in mechanisms of addressing T regulatory cell-inducing signals useful for promoting immune tolerance
- Increased IL-10 and Foxp3 induction in cord blood mononuclear cells of non-atopic compared to atopic mothers, may indicate an increased capacity to respond to microbial stimuli.
- The data support the conclusion that the neoplastic cells in CTCL do not express the T(reg) marker FOXP3.
- The finding of reduced endometrial Foxp3 implicates impaired differentiation of uterine T cells into the Treg phenotype as a key determinant of fertility in women.
- These data are the first to demonstrate differences in function and FOXP3 expression of CD4(+)CD25(+) T cells from patients with RR- and SP-MS.
- Expression of Foxp3 in non-small cell lung cancer patients is significantly higher in tumor tissues than in normal tissues, especially in tumors smaller than 30 mm
- Most patients lacked FOXP3-expressing cells, further solidifying the association between FOXP3 deficiency and immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome.
- IL-2 treatment resulted in anincrease in FOXP3 expression in CD3+ T cells. CD56+CD3- natural killer (NK) cells in cancer.
- HTLV-1-associated myelopathy/tropical spastic paraparesis was associated with lower expression of Foxp3 in leukocytes; suggests impaired Foxp3 expression may contribute to development of inflammatory disease in HTLV-1 infection
- Regulatory T cells (T(regs)) containing FOXP3+ were increased in HIV patients after HAART therapy.
- These findings indicate that forkhead box protein P3 mutations in immune dysregulation, polyendocrinopathy, enteropathy, X-linked patients result in heterogeneous biological abnormalities, leading to a dysfunction in regulatory and effector T cells.
- Measurement of mRNA expression levels of specific marker FOXP3 in synovial fluid of rheumatic joints confirms the presence of regulatory CD25(bright)CD4+ T cells.
- The orderly regulation of trafficking receptors in FOXP3-positive T cells according to stages of differentiation and activation is potentially important for their tissue-specific migration and regulation of immune responses in humans.
- Prognostic significance of FOXP3-positive regulatory T cells in overall survival in follicular lymphoma.
- Differences in the level of FOXP3 expression in the conjunctiva may indicate a role for regulatory T cells in the resolution of the conjunctival immune response, which is important in protection from immunopathology of trachoma.
- polyendocrinopathy, enteropathy, X-linked syndrome (IPEX) mutations in these domains correlate with deficiencies in FOXP3 repressor function, corroborating their in vivo relevance
- CD4+ CD45RO+ Foxp3+ CD25hi T lymphocytes are highly proliferative, with a doubling time of 8 days, compared with memory CD4+ CD45RO+ Foxp3- CD25- (24 days).
- Here we show that levels of Foxp3 mRNA are increased in CD4+ T cells from HIV-infected patients responding to antiretroviral therapy.
- Foxp3 may regulate transcription through direct chromatin remodeling, and Foxp3 function is influenced by signals from the TCR
- Samples from the long-survival group were more likely than those from the short-survival group to have CD4+ staining cells and to have FOXP3-positive cells in a perifollicular location.
- Expression of endogenous FOXP3 in humans is not sufficient to induce regulatory T cell activity or to identify regulatory T (Treg) cells.
- Data showed that autologous bone marrow graft recipients whithout graft versus host disease (GVHD) had significantly higher FOXP3 compared to those with GVHD.
- assessment of Foxp3 mRNA inside an allograft may distinguish vascular from nonvascular rejection.
- In this review, a new role is suggested for FOXP3 in human CD4+ T cells: down-modulating responses to T cell receptor-mediated stimulation.
- Heme oxygenase-1 mRNA expression is linked to the induction of Foxp3 in CD4+ CD25+ glioma infiltrating regulatory T-cells.
- Mucosal Foxp3 mRNA levels and Foxp3+CD3+ cells were significantly reduced in transplant recipients using prednisone/azathioprine/tacrolimus compared with controls but no direct relationship between Foxp3 expression and 1 specific drug was detected.
- Abundant intraepithelial infiltrations of regulatory T cells with very high levels of Foxp3 expression was detected in five primary tumours.
- Regulatory T cells concentrate in tubules in kidney transplantation, contributing to FOXP3 mRNA in urine.
- FOXP3+ regulatory T cells affect the development and progression of hepatocarcinogenesis
- BCG vaccine-receiving tuberculosis patients showed increase in FOXP3 mRNA levels.
- The current study suggests that activated NK interfere with CD28-mediated Foxp3 protein and RNA expression in CD4(+)CD25(-) T lymphocytes.
- regulatory roles of T-cell receptor (TCR), co-stimulatory molecules, interleukin-2 (IL-2), transforming growth factor-beta (TGF-beta) and beyond pathways on Foxp3 expression
- This study reports that altered peripheral blood frequencies of Tregs, as defined by the expression of FOXP3, are not specifically associated with type 1 diabetes.
- Expression of FOXP3 is a normal consequence of CD4(+) T cell activation and can no longer be used as an exclusive marker of T regulatory cells.
- FOXP3 interactions with histone acetyltransferase and class II histone deacetylases are required for repression
- In natural T(R) cells, Foxp3 interacts physically with AML1
- The immunohistochemistry of FOXP3 is used in the rapid screening for IPEX syndrome.
- implicate Interleukin-10-producing CD25(-)Foxp3(-) T cells in the pathogenesis of human visceral leishmaniasis
- Analysis of cd4+ CD25+ regulatory T cells and FOXP3 mRNA in the peripheral blood of patients with asthma.
- These findings indicate that induction of FOXP3 is intrinsic to CD8 T cells that are activated in the presence of IL-2 or IL-15.
- Intrahepatic FOXP3 levels are associated with HCV reinfection, a history of acute rejection, and increased within the first year after liver transplantation.
- results suggest that polymorphisms of the FOXP3 gene may play a role in the genetic susceptibility to autoimmune thyroid diseases in Caucasians, perhaps by altering FOXP3 function and/or expression
- NFAT1 could explain low FOXP3 expression and diminished Treg frequency in aplastic anemia.
- Phenotypic Foxp3+ Tregs, in conjunction with immature dendritic cells and Th2 cytokines, suggests an attenuated state of immunity to human basal cell carcinoma.
- study failed to find an association between SNPs in the FOXP3 gene region and Juvenile Idiopathic Arthritis
- Posttransplantation, the FOXP3 mRNA levels were higher in endomyocardial biopsies assigned to a higher International Society for Heart and Lung Transplantation rejection grade.
- Our data demonstrate that FOXP3 is an X-linked breast cancer suppressor gene and an important regulator of the HER-2/ErbB2 oncogene.
- Exposure of peripheral blood mononuclear cells to melanoma results in induction of FOXP3(+) T(reg) cells.
- Peritransplanat donor vertebral body bone marrow cells have higher 10-year renal transplant acceptance, chimerism, and FoxP3 mRNA in unclarified regulatory cell phenotypes.
- This study showed no association between microsatellite polymorphism in the promoter region of FOXP3 gene and susceptibility to type 1 diabetes in the Japanese population, though examination in larger samples is preferred to confirm this result.
- reveal a novel role for non-Hodgkin lymphoma B cells in the development of intratumoral regulatory T cells
- The T regulatory (Treg) cell-defining transcription factor FOXP3 in cooperation with NF-AT promotes TLR1- gene expression.
- We have identified the FOXP3 gene in juvenile Graves' disease.
- Essential transcription factor not only for differentiation and function of naturally occurring Treg cells but also for regulation of intracellular molecules related to effector T-cell responses. Review.
- FOXP3 DNA demethylation constitutes the most reliable criterion for natural regulatory T cells available at present
- analysis of FOXP3-transduced Jurkat-T cells as regulatory T (Treg)-like cells
- FOXP3 has a role in IPEX syndrome [review]
- CD4+CD25+CTLA-4+FoxP3+ T cells have roles in patients with systemic lupus erythematosus and are impaired after conventional treatments
- Regulatory T cells (Treg) suppress immune responses, making them an exciting therapeutic target for achieving operational transplant tolerance. FOXP3 is a master gene required for the development and function of Treg.
- Foxp3 expression in pancreatic carcinoma cells as a novel mechanism of immune evasion in cancer.
- proportions of FOXP3-bearing lymphocytes were higher in vertical than in radial growth phase, as well as in late than in early melanoma stages
- FOXP3+ CD4+ CD25(+high) regulatory T cells both in peripheral blood and in renal infiltrates were higher in donor-specific hyporesponders than in nonhyporesponders
- patients with FOXP3 gene mutations revealed a paucity of CD4(+)CD25(+)FOXP3(+) T cells.
- mechanism for IL-21-mediated expansion of antigen-specific CTLs that involves suppression of Foxp3-expressing cells and reversal of inhibition to tumor-associated antigen-specific cytotoxic T cell generation
- FoxP3 as a biomarker should be explored for human tumors to enable physicians to make better decisions in oncologic care and to prepare the field for novel therapeutic agents directed at the elimination of regulatory T cells within tumors.
- Foxp3+ cells can be detected in kidney transplant biopsies with acute rejection.
- Despite the expression of CTLA-4 and Foxp3, tumors were incapable of suppressing the proliferation of autologous T8 cells. ATL cells are phenotypically Treg cells in at least some patients, but lack immunoregulatory functions toward T8 cells.
- CD4+CD25highFoxp3+ T cells have a role in squamous cell carcinoma of the head and neck
- downregulation of SKP2 was critical for FOXP3-mediated growth inhibition in breast cancer cells that do not overexpress ERBB2/HER2.
- The ratio of FOXP3+ regulatory T-cells to granzyme B+ cytotoxic T/NK Cells predicts prognosis in classical Hodgkin lymphoma.
- Our results show the presence of CD25 FoxP3 T regulatory cells in chronic atopic dermatitis lesions
- in contrast to intragraft FOXP3 gene expression, the peripheral FOXP3 mRNA levels lack correlation with anti-donor immune responses in the graft. FOXP3 does not appear to be a candidate gene for non-invasive diagnosis of non-responsiveness or rejection.
- CD8+FOXP3+ T cells play an important role in unresponsiveness related to upregulated interleukin receptors on dendritic cells.
- There is an accumulation of FoxP3-expressing regulatory T cells in RA SF, and such recruitment may be dependent on the distinct chemokine receptors expressed on regulatory T cells.
- Homozygous loss of function of foxp3 gene results in the absence of development of a crucial subpopulation of lymphocytes with CD4+CD25+ phenotype, called regulatory T-cells. [REVIEW]
- LPS-activated monocytes suppress T cell immune responses and induce FOXP3 expression in resting CD4+CD25- T cells through a COX-2-PGE2-dependent mechanism.
- interleukin 4 (IL-4) present at the time of T cell priming inhibits FOXP3
- Forkhead transcription factor 3 (FoxP3) expression and T(reg) cell suppression were greater in patients with acute HCV infection , 6 months later, the resolution of disease was associated with a relative loss of functional suppression
- FOXP3 expression was found in some CD4(+) T cells and CD25(+) cells but not in CD8(+) T cells. FOXP3(+) T cells in periodontitis lesions can be considered to be effector T cells.
- TNreg cells are precursors for human Treg cells; these cells require a high level of FoxP3 expression to maintain their suppressive function.
- higher percentages of FOXP3-positive Tregs on initial tumor biopsy evidenced a significantly longer OS
- Tissue samples at different points showed a significant reduction in IL-1beta mRNA expression, and a significant increase in Foxp3 mRNA expression in ulcerative colitis.
- FOXP3 expression in adult T-cell leukemia/lymphoma and reflects morphological features and is clinically and pathologically associated with an immunosuppressive state.
- Campath-1H (Alemtuzumab) is an effective immunodepletion agent used in renal transplantation which increass FOXP3 regulatory T cells.
- After stimulation of CD4+CD25- T cells, the cells express FOXP3 display potent immunosuppressive properties.
- activation of STAT5 sustains FOXP3 expression in both Treg and Teff cells and contribute to our understanding of how cytokines affect the expression of FOXP3
- After culture with mesenchymal stromal cells (MSCs) both immunoselected fractions registered increases in the CD4(+)/CD25(bright)/FoxP3 expression was downregulated.
- The unique FOXP3 promoter methylation profile in Tregs suggests that a demethylated pattern is a prerequisite for stable FOXP3 expression and suppressive phenotype
- B7-H1, PD-1 and FOXP3 may have roles in progression of breast neoplasms
- Higher FoxP3 expression at diagnosis predicted worse future glycemic control while higher mean numbers of IL-10 cells were associated with better future glucose control.
- Immunodysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome is a rare disorder caused by mutations in the FOXP3 gene
- IL2/FOXP3-dependent negative feedback loop that normally regulates the T cell immune response
- FOXP3 expression in cutaneous and systemic CD30-positive lymphoproliferations is generally confined to tumour infiltrating rgulatory T-lymphocytes
- expand the possible targets of FOXP3-mediated repression and demonstrate functional differences between FOXP3 isoforms
- the decision of antigen-stimulated cells to differentiate into either T(H)17 or T(reg) cells depends on the cytokine-regulated balance of RORgammat and Foxp3
- FOXP3-independent mechanisms, mediated by IL-10, contribute to the induction and suppressor functions of type 1 regulatory T cells
- Both Foxp3 isoforms possess similar capacities to induce Treg. However, unnaturally high expression levels are required to convey Treg functions to CD4(+)CD25(-) cells.
- The level of expression of FOXP3 was normal in Treg cells from patients with SLE.
- FoxP3, a key regulator of immune suppression, is not only expressed by regulatory T cells but also by melanoma cells, Epstein Barr virus-transformed B cells, and a wide variety of tumor cell lines.
- Foxp3 can regulate pim 2 expression.
- Foxp3 mRNA as well as Foxp3 protein was detected in all tumor cell lines, correlating with the expression levels of IL-10 and TGFb1
- Foxp3 inhibits RORgammat-mediated IL-17A mRNA transcription through direct interaction with RORgammat
- Although the FOXP3 gene polymorphism has no effect on susceptibility to sarcoidosis, the (GT)15 allele may exert protective effects against skin involvement.
- FOXP3 expression did not correlate with favorable graft outcomes, even when the analysis was restricted to biopsies with rejection
- Foxp3 in normal T cells, but not mRNA, is basically potent at discriminating a subset of Treg cells from CD25(+) T-cell populations, in leukemic T cells could be implicated in oncogenesis and has a potentially useful clinical role.
- The correlation between the presence of FOXP3(+) Tregs and high vessel density in endometrial adenocarcinomas suggests a link between immunity, intratumoral angiogenesis and poor prognosis.
- FoxP3(+) Treg cells are productively infected and play an important role in acute HIV-1 infection in vivo
- Preservation of FoxP3+ regulatory T cells in the peripheral blood of HIV-1-infected elite suppressors correlates with low CD4+ T-cell activation.
- results, demonstrating that FOXP3 expression driven solely by the CD28/B7 interaction inhibited T cell activation, support the role of CD28 in the regulation of peripheral tolerance and suggest a new mechanism through which it could occur
- GARP is a regulatory T cell specific cell surface molecule that mediates suppressive signals and induces Foxp3 expression
- IRF-1 is a key negative regulator of CD4(+)CD25(+) Treg cells through direct repression of Foxp3 expression
- acquisition of suppressive behavior by activated CD4(+)CD25(-) T cells requires the expression of CTLA-4, a feature that appears to be facilitated by, but is not dependent on, expression of FoxP3
- H. pylori-positive patients revealed a high induction of FOXP3 transcript which correlated positively with inflammation and TGF-beta1 levels.
- Foxp3 has a role in preventing progression toward acute rejection of kidney transplants
- There were fewer numbers of Foxp3+ T cells in the monoclonal variants of pityriasis lichenoides chronica and pigmented purpuric dermatosis.
- malignant T cells express low molecular splice forms of FOXP3 and function as Tregs
- FoxP3+ peripheral T-cell lymphomas not otherwise specified presumably derived from bona fide Treg cells occurs but seems rare in the Western population
- Foxp3+ T-regulatory cell frequency in the minor salivary glands lesions of Sjogren's syndrome patients correlates with inflammation grade and certain risk factors for lymphoma development.
- FOXP3 decreases binding of NFAT2 to the HIV-1 LTR in vivo
- Effects of natalizumab treatment on FOXP3 T regulatory cells is reported.
- The kinetics of FOXP3 T-cell accumulation during a human cutaneous antigen-specific memory response in vivo are reported.
- CD49d provides access to highly pure populations of untouched Foxp3(+) Treg cells conferring maximal safety for future clinical applications
- FOXP3 protein expression did not correlate with disease severity.
- Children with type 1 diabetes show decreased induction of FOXP3 in T cells.
- Evidence is provided that the increase of CD4+CD25 high T cells and FoxP3 transcripts is associated with operational tolerance in liver transplanted patients during immunosuppression withdrawal.
- FOXP3 acts as a quantitative regulator rather than a simple molecular switch for Treg
- the (GT)n microsatelloite polymorphism in the FOXP3/Scrufin gene was associated with Japanese adult onset type 1 diabetes, especially in females, and slowly progressive type 1 diabetes.
- cervical mRNA expression of IFN-gamma, IL-10, and IL-12, as well as the Treg transcription factor Forkhead box P3 (Foxp3), in a cohort of young women showed elevated Foxp3 expression.
- First report showing that Foxp3 cells are present within grafts in a subset of tolerant patients after human liver transplantation.
- The prevalence of Foxp3-positive Tregs and dendritic cells was significantly higher in squamous cell carcinoma and Bowen's disease than in actinic keratosis.
- Children with only T1 diabtes mellitus generally showed a lower FOXP3 mRNA expression than did children with celiac disease (CD), or with T1D in combination with CD.
- Signal transducer and activator of transcription (STAT)1 binding elements found within the proximal part of the human foxp3 promoter function as a key regulatory unit for promoting foxp3 gene expression.
- This study shows the possible role of FoxP3 in the development of tissue characteristic humoral immunity in type 1 diabetes.
- demonstrates an association between donor-specific transfusions and FoxP3+ T cells
- Our data indicate that FOXP3 is functional in nonallergic healthy donors as well as allergic patients, and FOXP3-expressing T cells may be responsible for the down-regulation of allergen-specific T-helper responses in individuals.