Department of Medicinal Chemistry and Institute for Translational Neuroscience, University of Minnesota, 308 Harvard Street SE, Minneapolis, Minnesota 55455, United States.
Departments of Pharmacodynamics and Medicinal Chemistry, University of Florida, Gainesville, Florida 32610, United States.
ACS Chem Neurosci. 2021 Feb 3;12(3):542-556. doi: 10.1021/acschemneuro.0c00755. Epub 2021 Jan 20.
The melanocortin receptors (MCRs) are important for numerous biological pathways, including feeding behavior and energy homeostasis. In addition to endogenous peptide agonists, this receptor family has two naturally occurring endogenous antagonists, agouti and agouti-related protein (AGRP). At the melanocortin-4 receptor (MC4R), the AGRP ligand functions as an endogenous inverse agonist in the absence of agonist and as a competitive antagonist in the presence of agonist. At the melanocortin-3 receptor (MC3R), AGRP functions solely as a competitive antagonist in the presence of agonist. The molecular interactions that differentiate AGRP's inverse agonist activity at the MC4R have remained elusive until the findings reported herein. Upon the basis of homology molecular modeling approaches, we previously postulated a unique interaction between the D189 position of the hMC4R and Asn114 of AGRP. To further test this hypothesis, six D189 mutant hMC4Rs (D189A, D189E, D189N, D189Q, D189S, and D189K) were generated and pharmacologically characterized resulting in the discovery of differences in inverse agonist activity of AGRP and an 11 macrocyclic compound library. These data support the hypothesized interaction between the hMC4R D189 position and Asn114 residue of AGRP and define critical ligand-receptor molecular interactions responsible for the inverse agonist activity of AGRP at the hMC4R.
黑皮质素受体(MCRs)在许多生物学途径中都很重要,包括摄食行为和能量平衡。除了内源性肽激动剂外,该受体家族还有两种天然存在的内源性拮抗剂,即刺鼠相关蛋白(AGRP)。在黑皮质素-4 受体(MC4R)上,AGRP 配体在没有激动剂的情况下作为内源性反向激动剂,在有激动剂的情况下作为竞争性拮抗剂。在黑皮质素-3 受体(MC3R)上,AGRP 在有激动剂的情况下仅作为竞争性拮抗剂发挥作用。直到本文报道的研究结果,区分 AGRP 在 MC4R 上的反向激动剂活性的分子相互作用仍然难以捉摸。基于同源分子建模方法,我们之前假设 hMC4R 的 D189 位置与 AGRP 的 Asn114 之间存在独特的相互作用。为了进一步验证这一假设,我们生成了六个 D189 突变 hMC4Rs(D189A、D189E、D189N、D189Q、D189S 和 D189K)并进行了药理学表征,结果发现 AGRP 和 11 个大环化合物文库的反向激动剂活性存在差异。这些数据支持 hMC4R 的 D189 位置与 AGRP 的 Asn114 残基之间的假设相互作用,并定义了负责 AGRP 在 hMC4R 上的反向激动剂活性的关键配体-受体分子相互作用。