from the brain region-specific glycosylation of Asn residues and/or different N-glycan compositions attached to the Asn residues. Thus, a likely explanation for our observation is that the A118G/A112G mutation leads to brain area-specific changes in N-glycan contents and thereby differentially affects protein expression of MOPR across brain regions. Similarly, the median Mr's of the A118/N40-hMOPR and the G118/D40-hMOPR are higher in HEK 293 cells than in CHO cells (Fig. 4), suggesting higher levels of glycosylation in HEK293 cells. However, how the extents and types of glycosylation affect glycoprotein expression are not well understood.
