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Vollum Institute (D.L., R.D.C.) Oregon Health Sciences
University Portland, Oregon 97201
Department of Animal
Science (D.I.V.) Agricultural University of Norway N-1432 As,
Norway
Dark coat color in the mouse and fox results from
constitutively activated melanocortin-1 receptors. Receptor mutations
in the mouse (E92K, L98P), cow (L99P), fox (C125R), and sheep (D119N)
cluster near the membrane/extracellular junctions of the second and
third transmembrane domains, an acidic domain that is the likely site
of electrostatic interaction with an arginine residue in the ligand,
-MSH. For transmembrane residues E92, D119, and C125, conversion to
a basic residue is required for constitutive activation. Unlike
constitutively activating mutations in many G protein-coupled receptors
that increase agonist efficacy and affinity, these MC1-R mutations have
the opposite effect. Therefore, these mutations do not activate the
receptor by directly disrupting intramolecular constraints on formation
of the active high-affinity state, R*, but do so indirectly by
mimicking ligand binding.
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