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NKX2-3 encodes a homeodomain-containing transcription factor. Additionally we are shipping NK2 Homeobox 3 Antibodies (18) and many more products for this protein.
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NKX2-3 is a key mediator for maintaining myofibroblast characteristics, and our results show that colorectal myofibroblasts, as defined by the expression of AOC3 (show AOC2 Proteins), NKX2-3, and other markers, are a distinctly different cell type from TGFbeta (show TGFB1 Proteins)-activated fibroblasts
The persons with a NKX2-3 G or T allele may have a moderately increased risk of CD.
NKX2-3 may play different roles in ulcerative colitis and Crohn's disease pathogenesis by differential regulation of EGR1 (show EGR1 Proteins).
A positive correlation was observed between mRNA expression of PTPN2 and NKX2-3 in B cells and in intestinal tissues from both Crohn's disease and ulcerative colitis patients.
The binding of NFAT1 to the NKX2-3 promoter region with rs1190140 was confirmed by chromatin immunoprecipitation assay.
the risk haplotype of NKX2.3 confers susceptibility to UC through increasing expression of NKX2.3 mRNA in the colonic mucosa.
NKX2-3 may play an important role in inflammatory bowel disease pathogenesis by regulating endothelin-1 and VEGF signaling in human intestinal microvascular endothelial cells.
Data suggest that NKX2-3 and IRGM (show IRGM Proteins) are susceptibility loci for inflammatory bowel disease in Eastern European patients.
Nkx2-3 may contribute to the pathogenesis of inflammatory bowel disease-associated colorectal cancer and sporadic colorectal cancer by regulating the Wnt (show WNT2 Proteins) signaling pathway.
a decrease in Nkx2-3 gene expression level can profoundly alter the expression of genes and cellular functions relevant to the pathogenesis and progression of inflammatory bowel disease, such as EDN1 (show EDN1 Proteins).
Nkx2-3 deficiency reprograms the endothelial addressin preference for lymphocyte homing in Peyer's patches.
the organ-specific patterning of splenic vasculature is critically regulated by Nkx2-3, thereby profoundly affecting the lymphocyte homing mechanism and blood filtering capacity of the spleen in a tissue-specific manner.
The splenic vascular defects in Nkx2-3 deficiency include the generation of LYVE-1 (show LYVE1 Proteins)(+) cysts, comprised of endothelial cells without being committed along the LEC lineage.
NKX2.3 has a role in mouse pharyngeal organogenesis
Data indicate a substantial role for Nkx2-3 in the correct association of lymphocytes and splenic stromal elements that is independent of chemokine (show CCL1 Proteins) expression.
Phenotypic heterogeneity among different vascular elements within distinct anatomical regions of the spleen differentially depends on developmental factors such as lymphotoxin (show LTB Proteins) signaling or Nkx2.3, whereas the marginal sinus is controlled by both pathways.
Formation of various white pulp fibroblast subsets is differentially affected by the presence of Nkx2.3 activity, possibly also influencing their role in various immune functions linked with complement activation and deposition.
This gene encodes a homeodomain-containing transcription factor. The encoded protein is a member of the NKX family of homeodomain transcription factors. Studies of similar proteins in mouse and rat have indicated a potential role in cellular differentiation.
NK2 transcription factor related, locus 3
, homeobox protein NK-2 homolog C
, homeobox protein Nkx-2.3
, Drosophila NK2 transcription factor related, locus 3
, homeobox protein NK-2 homolog 3