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Kenakin, T.

Publications and source records attributed to Kenakin, T..

2 recordsLinked to original sources

Differential effects of sodium on agonist-induced conformational transitions and signaling at μ and κ opioid receptors

Sodium ions are classically conceptualized as negative allosteric modulators for G protein coupled receptors (GPCRs), although there have been reports of either positive allosteric modulation or no effect of sodium on GPCR function. Here we identified opposing actions of sodium on the and {kappa} opioid receptors. We utilized a variety of methods including radioligand binding, real-time conformational monitoring of transitions using bioluminescence resonance energy transfer and signaling assays using the TRUPATH resource. At the receptors, sodium behaved as a negative allosteric modulator of binding, conformational transitions and signaling. Intriguingly, bitopic agonists were unaffected by sodium concentrations. By contrast, at the {kappa} opioid receptor sodium negatively modulated agonist binding and positively modulated conformational transitions and signaling. Taken together, these findings support the notion that the differential sensitivities to sodium concentrations will result in opposing effects on cell surface and intracellular signaling.

neuroscience↗

Neurotensin receptor allosterism revealed in complex with a biased allosteric modulator

The NTSR1 neurotensin receptor (NTSR1) is a G protein coupled receptor (GPCR) found in the brain and peripheral tissues with neurotensin (NTS) being its endogenous peptide ligand. In the brain, NTS modulates dopamine neuronal activity, induces opioid-independent analgesia, and regulates food intake. Recent studies indicate that biasing NTSR1 toward {beta}-Arrestin signaling can attenuate the actions of psychostimulants and other drugs of abuse. Here we provide the cryoEM structures of NTSR1 ternary complexes with heterotrimeric Gq and Go with and without the brain penetrant small molecule SBI-553. In functional studies, we discovered that SBI-553 displays complex allosteric actions exemplified by negative allosteric modulation for G proteins that are G subunit selective and positive allosteric modulation and agonism for {beta}-Arrestin translocation at NTSR1. Detailed structural analysis of the allosteric binding site illuminated the structural determinants for biased allosteric modulation of SBI-553 on NTSR1. These insights promise to both accelerate the structure-guided design of more effective NTSR1 therapeutics and provide insights into the complexities of GPCR allosteric modulation.

biophysics↗