ArticleMethods in molecular biology (Clifton, N.J.)2010
Molecular assays for characterization of alternatively spliced isoforms of the u opioid receptor (MOR).
Article in Methods in molecular biology (Clifton, N.J.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 8 citations in OpenAlex.
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5 authors at 1 institution in 1 country.
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Abstract
Mu-opioid receptor (MOR) belongs to a family of heptahelical G-protein-coupled receptors (GPCRs). Studies in humans and rodents demonstrated that the OPRM1 gene coding for MOR undergoes extensive alternative splicing afforded by the genetic complexity of OPRM1. Evidence from rodent studies also demonstrates an important role of these alternatively spliced forms in mediating opiate analgesia via their differential signaling properties. MOR signaling is predominantly G(ia) coupled. Release of the alpha subunit from G-protein complex results in the inhibition of adenylyl cyclase/cAMP pathway, whereas release of the betagamma subunits activates G-protein-activated inwardly rectifying potassium channels and inhibits voltage-dependent calcium channels. These molecular events result in the suppression of cellular activities that diminish pain sensations. Recently, a new isoform of OPRM1, MOR3, has been identified that shows an increase in the production of nitric oxide (NO) upon stimulation with morphine. Hence, there is a need to describe molecular techniques that enable the functional characterization of MOR isoforms. In this review, we describe the methodologies used to assay key mediators of MOR activation including cellular assays for cAMP, free Ca(2+), and NO, all of which have been implicated in the pharmacological effects of MOR agonists.
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