anti-FOXP3 (FOXP3) 抗体产品概述

Zebrafish Forkhead Box P3 (FOXP3) interaction partners

1. analysis of Foxp3-based immunoregulation and autoimmunity in zebrafish

2. correlation between the expression of t-bet, stat6 and foxp3 with other genes involved in Th and T(reg) responses

Atlantic Salmon (Salmo salar) Forkhead Box P3 (FOXP3) interaction partners

1. cloning and characterization of the full-length cDNA of Atlantic salmon Foxp3, which possesses a Forkhead domain, a zinc finger domain and a leucine-zipper domain as its counterpart in mammals

Human Forkhead Box P3 (FOXP3) interaction partners

1. Consistent with iNOS and Foxp3 expression, TGFbeta, CTLA-4 and IL-10 were significantly related to the tumor stage progression.

2. Because loss of FOXP3 transcriptionally induces c-Myc expression and loss of TSC1 activates mTOR signaling, these data suggest cross-talk between FOXP3-c-MYC and TSC1-mTOR signaling that converges on c-MYC to regulate tumor progression

3. This study suggests that Foxp3 and miR-146a regulate the progression of oral lichen planus by negatively regulating TRAF6, which may provide a promising therapeutic target for oral lichen planus treatment.

4. This is the first report providing detailed evidence showing that frequency and FOXP3 expression of CD8+CD25High+ T cells were upregulated in the peripheral blood of hepatocellular carcinoma patients and this expansion is positively correlated with worse prognostic markers as alpha-fetoprotein and hepatic focal lesions.

5. Foxp3 single nucleotide polymorphisms might increase Crohn's disease susceptibility by reducing the colonic expression of Foxp3 in Chinese male patients.

6. The CD4+ CD25+ regulatory T cells function defect in GD patients is mediated by the abnormal acetylation of FOXP3, which is regulated by miR-23a-3p via targeting SIRT1.

7. These data demonstrate that sitagliptin in combination with VitD3 may accelerate the process of T2DM treatment by exerting synergic anti-inflammatory effects on immune system through upregulation of FOXP3 and IL-37, and downregulation of RORgammat and BCL6 as well as IFN-gamma, IL-17 and IL-21 production.

8. excreted-secreted antigens (ESA) directly influenced the expression of IL-2Rgamma, rather than the availability of IL-2 indirectly. ESA suppressed the level of Foxp3 via inhibiting IL-2Rgamma/JAK3/Stats signaling pathway in EL4 cells.

9. Foxp3 deficiency dysregulates metabolic checkpoint kinase mammalian target of rapamycin (mTOR) complex 2 (mTORC2) signaling and gives rise to augmented aerobic glycolysis and oxidative phosphorylation.

10. FOXP3 is confirmed to have the capacity to suppress proto-oncogene MYC in liver neoplasm by up-regulating miR-198 through binding to its promoter, while miR-198 targets the 3'-UTR of MYC mRNA to inhibit its translation. The high expression of FOXP3 and, especially miR-198, is verified to have strong suppression on liver tumor cells viability and proliferation, while promoting apoptosis.

11. Human peripheral blood CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) express membrane-bound TNF.

12. The combination of low budding, low stromal FOXP3 counts, presence of tertiary lymphoid tissue (TLT), and absence of CDKN2A mutations confers significant survival advantage in patients with pancreatic ductal adenocarcinoma (PDAC)

13. Results show that FOXP3 expression in T-regulatory cells is regulated by YAP1.

14. Immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome is an autoimmune disease caused by mutations in the forkhead box protein 3 gene (FOXP3). Five out of 22 identified FOXP3 mutations have not been described yet: c.-23 + 1G > A, c.-23 + 5G > A, c.264delC, c.1015C > T and c.1091A > G. The first two produced atypical, attenuated phenotypes.

15. systematic review and meta-analysis of rs3761548 and rs2232365 polymorphism and multiple sclerosis susceptibility

16. FOXP3 Inhibitory Peptide P60 Increases Efficacy of Cytokine-induced Killer Cells.

17. cancer cell-derived Foxp3 contributed to Tregs expansion in tongue squamous cell carcinoma microenvironment with positive and negative feedbacks

18. this study shows that single nucleotide polymorphisms in the FOXP3 gene are associated with viral load and liver enzyme levels in patients with chronic hepatitis B and chronic hepatitis C

19. CD3+CD4+LAP+Foxp3-Tregs limit the extension of inflammatory lesions in UC patients.

20. Foxp3 Molecular Dynamics in Treg in Juvenile Idiopathic Arthritis.

Mouse (Murine) Forkhead Box P3 (FOXP3) interaction partners

1. Authors also show that despite their sustained expression of Foxp3, Blimp-1(-/-) RORgammat(+)IL-17-producing Treg lose suppressor function and can promote intestinal inflammation, indicating that repression of Th17-associated cytokines by Blimp-1 is a crucial requirement for RORgammat(+) Treg function.

2. OX40 can also activate the AKT-mTOR pathway, especially in the absence of BATF3 and BATF, to inhibit Foxp3 induction.

3. The results identify a novel role for ICOS costimulation in imprinting the functional stability of Foxp3 that is required for the retention of full Treg cell function in the periphery.

4. Findings indicate a direct role for Foxp3 in suppressing Th2-like Treg cells.

5. These results suggest that murine extrathymic Foxp3+ DP T cells may represent a unique regulatory T cell subset.

6. CCAAT/enhancer-binding protein (C/EBP) functions as a safeguard that enhances Treg cell generation by dampening the inhibitory effect of IFN-gamma and IL-4 on Foxp3 expression.

7. Function of Central and Effector Foxp3(+) Regulatory T Cells.(

8. Results found Foxp3 is both necessary and sufficient to program Treg-increased respiratory capacity and ability to utilize fatty acids (FA) to fuel oxidative phosphorylation. Foxp3 drives upregulation of components of all the electron transport complexes, increasing their activity and ATP generation by oxidative phosphorylation. FA beta-oxidation also results in selective protection of Foxp3(+) from FA-induced cell death.

9. Study found that a large number of Foxp3-bound genomic sites in Treg cells were occupied by Foxp1 in both Treg cells and conventional T cells. In Treg cells, Foxp1 markedly increased Foxp3 binding to these sites. These results suggest that Foxp1 serves an essential non-redundant function in Treg cells by enforcing Foxp3-mediated regulation of gene expression and enabling efficient IL-2 signaling in these cells.

10. study dissects time-dependent mechanisms behind Foxp3-driven T-cell regulation and establishes the Foxp3-Tocky system as a tool to investigate the mechanisms behind T-cell immunotherapies.

11. Destabilized FOXP3-EZH2 protein interaction via diverse mechanisms and consequent Treg abnormality may drive gastrointestinal inflammation.

12. Induction of CD4(+)CD25(+)FOXP3(+) regulatory T cells by mesenchymal stem cells is associated with modulation of ubiquitination factors and Treg-specific demethylated region demethylation.

13. Overall, these findings contribute to our understanding of the molecular mechanisms underlying the process of Foxp3 induction and may provide a rational basis for generating phenotypically and functionally stable iTreg cells.

14. Here we focus on the cytokines implicated in thymic development of Treg(T lymphocytes (Treg) expressing the transcription factor Foxp3), with a particular emphasis on the roles of interleukin-2 and IL-15

15. It has been shown that T-cell receptors-activated post-translational modification by O-linked N-Acetylglucosamine stabilizes FOXP3 and activates STAT5, thus integrating these critical signaling pathways.

16. This study demonstrated that adoptive transfer of CD4(+)CD25(+) Tregs can decrease mouse enteritis. Foxp3 expression may be improved through the Smad3 and NFAT2 signalling pathways.

17. FOXP3 represses the ability of hnRNPF to bind to its target pre-mRNA and thus modulates RNA alternative splicing

18. the strength of TCR stimulation is a key factor for induction of the demethylation of Foxp3 conserved non-coding sequence 2 and the generation of stable Tregs

19. Stable Foxp3 expression in extrathymically induced regulatory T cells (iTreg) requires Forkhead box protein P1 (Foxp1). Foxp1 binds a promoter region and genetic elements, including three CNSs (CNS1-3) downstream of the transcriptional start site of Foxp3 to preserve permissive histone modifications.

20. Epigenetic modification is also thought to take essential part into the upregulation of Foxp3 from naive CD4 + Tcells.

Pig (Porcine) Forkhead Box P3 (FOXP3) interaction partners

1. sequenced the entire Foxp3 cDNA which is 1296 nucleotides in length and codes for a polypeptide of 432 amino acids

2. In a miniature swine lung transplantation model, the FOXP3 mRNA level in the peripheral blood was upregulated at an early phase of rejection

Cow (Bovine) Forkhead Box P3 (FOXP3) interaction partners

1. GWAS identified a maternal variant in the upstream region of FOXP3 that was associated with infertility in repeat-breeding Japanese Black cattle that failed to conceive using embryo transfer. The variant affected the level of FOXP3 mRNA expression.

2. Experimental infection with bovine viral diarrhea virus did not provide evidence ofTreg activation based on expression of FoxP3 and CTLA4.

3. regulatory role in intramuscular fat deposition

4. The expression of Foxp3 in CD4(+) T cells from persistent lymphocytotic cattle was significantly increased.

5. There is a positive correlation between the intensity of CD25 expression and the expression of the transcription Foxp3 factor in bovine CD8(+) cells.

6. identification of Foxp3 expression in Treg cells

7. These findings revealed that despite the existence of a distinct bovine CD4(+)CD25(high) T cell population, which showed Foxp3 transcription/expression, natural regulatory activity did not reside in this cell population

Horse (Equine) Forkhead Box P3 (FOXP3) interaction partners

1. The correlation of TH17-related TLR4 expression and Foxp3-positive cells in the rectal tissue of horses with inflammatory bowel disease is reported.

2. Expression levels of FOXP3 mRNA copy numbers were significantly increased in lesional compared to tumour-distant samples. There was no difference in FOXP3 expression in tumour-distant samples from equine sarcoid- compared with control horses.

3. results confirm FoxP3 expression in the horse, in contrast to the mouse, is regulated similarly to FOXP3 expression in humans and provide evidence that FoxP3 expression by conventional T cells may help regulate the developing immune response