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Chunk #29 — Discussion — Decreased Mr of MOPR by A118G/A112G is indicative of its reduced N-glycosylation

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A common single nucleotide polymorphism A118G of the μ opioid receptor alters its N-glycosylation and protein stability.
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We found by immunoblotting that G112/D38-MOPR (G/G mice) had lower Mr than A112/N38-MOPR (A/A mice) in the thalamus, which is consistent with our previous report [18]. In addition, we demonstrated a similar difference in Mr of the MOPRs in the striatum (Fig.2). In addition, in stable cell lines G118/D40-hMOPR had lower Mr than A118/N40-hMOPR (Fig. 4). The findings that following deglycosylation with PNGase F, both variants of the hMOPR or the mouse MOPR had the same Mr (Fig. 3 and Fig. 5) support the notion that the decreases in Mr of the MOPR by the A118G or A112G SNP are due to varied N-glycosylation status, which may imply the elimination of one of the N-linked glycans by the SNP. It has been demonstrated that, in general, glycoproteins from the human brain show similar profiles of brain region-specific N-glycans as those from mouse and rat brains [34]. Therefore, what we observed on the MOPRs in the mouse brains is likely to reflect those in the human brain.