Receptor bias: difference between revisions
Diff·revision 4 → 5·18:58, 22 Oct 2024
Difference between revision 4 and revision 5 of Receptor bias. 2 lines changed; the page grew by 250 bytes.
| Revision 4 — 20:28, 9 Oct 2024 ProglucagonPia (talk) give the fasting and postprandial concentrations with the assay named 2,105 bytes +167 | Revision 5 — 18:58, 22 Oct 2024 CommaCarys (talk) fix the anchor on an internal link 2,355 bytes +250 | ||
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| 10 | At the [[GLP-1 receptor]] the pathways usually compared are cAMP accumulation, which mediates the insulinotropic effect, and β-arrestin recruitment, which terminates G-protein signalling and drives receptor internalisation.{{r|jones2018}} | 10 | At the [[GLP-1 receptor]] the pathways usually compared are cAMP accumulation, which mediates the insulinotropic effect, and β-arrestin recruitment, which terminates G-protein signalling and drives receptor internalisation.{{r|jones2018}} |
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| + | 12 | Bias is quantified as a bias factor relative to a reference agonist, and the number depends on the reference chosen, the cell system, the readout and the incubation time. Bias factors from different publications are not comparable.{{r|kenakin2013}} | |
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| 12 | == The concept == | 14 | == The concept == |
| 13 | Classical receptor theory treats an agonist's effect as a single efficacy applied to a single pathway. Biased agonism replaces this with a vector: an agonist has an efficacy for each transducer, and the ratio between them is what "bias" names.{{r|kenakin2013}} | 15 | Classical receptor theory treats an agonist's effect as a single efficacy applied to a single pathway. Biased agonism replaces this with a vector: an agonist has an efficacy for each transducer, and the ratio between them is what "bias" names.{{r|kenakin2013}} |