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AIRE, which is phosphorylated on two specific residues near its N terminus, then binds to the F-box protein 3 (FBXO3 (show FBXO3 Proteins)) E3 ubiquitin ligase (show MUL1 Proteins). In turn, this SCF (show KITLG Proteins)(FBXO3 (show FBXO3 Proteins)) (SKP1 (show SKP1 Proteins)-CUL1 (show CUL1 Proteins)-F box) complex ubiquitylates AIRE, increases its binding to the positive transcription elongation factor b (P-TEFb (show CDK9 Proteins)), and potentiates its transcriptional activity.
this paper shows that genetic polymorphisms in AIRE do not contribute to the Graves' disease in Spain
This study supports the notion that AIRE mutation could specifically affect human insulin (show INS Proteins) gene expression in thymic epithelial cells through INS (show INS Proteins)-VNTR and subsequently induce either insulin (show INS Proteins) tolerance or autoimmunity.
androgen control of an intrathymic Aire-mediated tolerance mechanism contributes to gender differences in autoimmunity.
results indicate that in females, estrogen induces epigenetic changes in the AIRE gene, leading to reduced AIRE expression under a threshold that increases female susceptibility to autoimmune diseases.
The rs2075876 and rs760426 loci of the AIRE gene are associated with increased risk for rheumatoid arthritis among ethnic Han Chinese from ShaanXi.
The novel mutation of c.622G>T (p.G208W) in AIRE gene is associated autoimmune polyendocrinopathy syndrome type I.
AIRE-655GAIRE-230T haplotype could dramatically alter AIRE transcription.
In the current study, we demonstrate that AIRE activates the expression of transiently transfected luciferase reporters that lack defined promoter regions, as well as intron and poly(A) signal sequences.
These results suggest that Aire expression is inherent to all medullary thymic epithelial cells (mTECs) but may occur at particular stage(s) and/or cellular states during their differentiation, thus accounting for the broad impact of Aire on the promiscuous gene expression of mTECs.
we found that Aire up-regulated TLR3 (show TLR3 Proteins) expression and modulated the downstream cytokine expression and nuclear factor-kappaB (NF-kappaB (show NFKB1 Proteins)) of the TLR3 (show TLR3 Proteins) signaling pathway.
Aire-expressing dendritic cells inhibited TCR signaling pathways and decreased quantity of CD4 (show CD4 Proteins)+IFN-gamma (show IFNG Proteins)+ autoreactive T cells. Aire plays role in maintenance of peripheral immune tolerance.
Aire may have a role in inducing Th1 (show HAND1 Proteins) and Th17 differentiation by upregulating cytokine expression in dendritic cells.
Our results identify Aire as an important regulator of peripheral T cell homeostasis in gastrointestinal tissues. Given a suitable trigger the absence of peripheral Aire leads to dysregulated T cell proliferation and disease.
Data indicate a highly conserved noncoding DNA element that is essential for Autoimmune regulator (Aire) gene expression.
Molecular characterization of the functional domains of Aire has revealed multiple binding partners that assist Aire's function in altering gene transcription and chromatin remodeling.
Aire expression in thymic epithelial cells was decreased in germ-free mice without commensal bacteria.
This gene encodes a transcriptional regulator that forms nuclear bodies and interacts with the transcriptional coactivator CREB binding protein. The encoded protein plays an important role in immunity by regulating the expression of autoantigens and negative selection of autoreactive T-cells in the thymus. Mutations in this gene cause the rare autosomal-recessive systemic autoimmune disease termed autoimmune polyendocrinopathy with candidiasis and ectodermal dystrophy (APECED).
, autoimmune polyendocrinopathy candidiasis ectodermal dystrophy protein
, autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)
, APECED protein homolog
, autoimmune polyendocrinopathy candidiasis ectodermal dystrophy protein homolog
, autoimmune regulator AIRE1a