This study demonstrates that DBA recognizes cyclically regulated epithelial glycans in both human and baboon endometrium. However, the timing of expression differs fundamentally in the two species, with abundant binding sites in the baboon in proliferative and early secretory phases, but appearance of such sites delayed in the human until the mid- and late secretory phases. In the baboon, the increased abundance of DBA sites in the late proliferative phase suggests regulation by estrogen, although more direct evidence will have to be sought to support this idea. In the human, there is already evidence that progesterone regulates production of DBA-binding glycans . In the baboon, the regulation by progesterone appears to be inhibitory (this study). flovent inhaler
High concentrations of GalNAc inhibit binding of DBA to target oligosaccharides. It binds to the Forssman-specific pentasaccharide GalNAca 1,3GalNAc(3 1,3Gala 1,4Gal|31, 4Glc-Cer , as well as to the fucosylated blood group A pentasaccharide GalNAca 1,3(Fuca1,2)Gal(31,4GlcNAc; other saccharides including GalNAcal,3Gal bind with lower affinity. Sialidase pretreatment greatly increased VVA binding but did not increase DBA binding to any significant degree, suggesting that chain capping (masking) does not explain the absence of sites in proliferative phase human endometrium. On the basis of these observations, the possibility was explored that variations in abundance of terminal aGalNAc could explain the changes in DBA binding.