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Given that GIPR antagonists cause retention of the receptor at the plasma membrane (prevent GIPR internalization [43]), perhaps the mere act of “stabilizing” the GIPR at the cell membrane makes maridebart cafraglutide less potent at producing cAMP via the GLP-1R than it would be if it did not interact with the GIPR at all
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The terms get used interchangeably in casual conversation, but they describe different steps in the workflow
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