This would appear to rule out the CRD directly binding to the ice (as the sugars would be competing ligands).
Family 1 UGTs usually utilize low molecular weight compounds as acceptor substrates and UDP-sugars as donors [ 12] and commonly possess a carboxy terminal consensus sequence (PSPG box) believed to be involved in binding to the UDP moiety of the sugar nucleotide donor [ 9, 15].
The agglutinating activity of SUL-III was most effectively inhibited by L-rhamnose and, to a lesser extent, by lactulose (Galβ1 → 4Fru) and lactose (Galβ1 → 4Glc), suggesting that the hydroxy group at C-1, C-2, and C-4 of the pyranose ring structure may influence sugar binding to the lectin (Table 1).
The simplest explanation is that GKA association with GK depends on sugar binding to the catalytic site and that the conformational change, as monitored by tryptophan fluorescence, is the result of cooperative binding of GKA and sugar.
Mannose-binding lectin (MBL) activates the lectin-complement pathway of innate immunity through binding to repetitive sugar arrays on microbial surfaces [ 1].
Via binding to sugar residues on the surface of pathogens, galectins are believed to play a role as pathogen recognition molecules [ 39].
Odorranalectin binding to monomeric sugar and glycoproteins did not require calcium.
Lectins binding to sugar structures of a membrane receptor can mimic or block the effect of the physiological ligand [ 48, 61, 62, 65, 77- 82].
The cells lit up in both cases, confirming that each lectin was binding to its preferred sugar.
