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Chunk #42 — 6. Species-specific SNPs in OPRM1: Spontaneous and generated — 6.2. Knock-in mouse model (A112G)

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OPRM1 SNP (A118G): involvement in disease development, treatment response, and animal models.
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that one consequence of the A112G knockin mouse (and the A118G SNP) is the deletion of an N-linked glycosylation site. Glycosylation plays a role in receptor sorting, expression, trafficking, ligand binding, and signal transduction (Fan et al., 1997; Rathz et al., 2002; Zhang et al., 2001); alterations in these processes could affect MOPR function in ways distinct from protein level changes.