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In laboratory models, IGF-1 LR3 has been observed to initiate stronger receptor activation than the parent molecule, potentially resulting in more robust cellular responses

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While GHSR1a constitutive activity is required for amplification of MC3R signaling, it has minimal effect on GHSR1a-MC3R dimer internalization, as treatment with the GHSR1a inverse agonist SP-analog only results in a small, nonsignificant reduction in internalization (Schellekens et al., 2013)