ArticleThe Journal of pharmacology and experimental therapeutics2010
Subcellular localization of mu-opioid receptor G(s) signaling.
Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Mu-opioid receptor and receptor tyrosine kinase crosstalk: Implications in mechanisms of opioid tolerance, reduced analgesia to neuropathic pain, dependence, and reward.Frontiers in systems neuroscience · 2022Review
- Review
- Components of the GTraffic (Copenhagen, Denmark) · 2020Article
- Chronic opioid treatment augments caveolin-1 scaffolding: relevance to stimulatory μ-opioid receptor adenylyl cyclase signaling.Journal of neurochemistry · 2016Article
- Ser/ Thr residues at α3/β5 loop of Gαs are important in morphine-induced adenylyl cyclase sensitization but not mitogen-activated protein kinase phosphorylation.The FEBS journal · 2012Article
- Formation of mu-/kappa-opioid receptor heterodimer is sex-dependent and mediates female-specific opioid analgesia.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
In membranes obtained from mu-opioid receptor (MOR) expressing Chinese hamster ovary (CHO) cells (MOR-CHO), the MOR-selective agonist sufentanil produced a concentration-dependent stimulation of guanosine 5'-O-(3-[35S]thio)triphosphate binding to G(s)alpha that was abolished by blocking MOR with naloxone. This unequivocally demonstrates the long-debated functionality of the previously described association of MOR with G(s)alpha. Several complementary observations indicate the relevance of caveolae to MOR-coupled G(s)alpha signaling. 1) In MOR-CHO membranes, sufentanil stimulated the translocation of G(s)alpha into Triton-insoluble membrane compartments. 2) Sufentanil enhanced the coimmunoprecipitation (co-IP) of G(s)alpha and adenylyl cyclase (AC) with caveolin-1 (a marker for caveolae) from the Triton-insoluble membrane fraction of spinal cord and MOR-CHO. 3) MOR blockade (via naloxone) or G(s) inactivation (via cholera toxin) abolished both the increased trafficking of G(s)alpha into the Triton-insoluble membrane fraction of MOR-CHO and the augmented co-IP from spinal cord membranes of G(s)alpha and AC with caveolin-1. This indicates that these events occurred subsequent to activation of MOR and G(s)alpha. Strikingly, lesser-phosphorylated G(s)alpha, which preferentially couple to MOR (Mol Brain Res 135:217-224, 2005; Mol Pharmacol 72:753-760, 2007; Mol Pharmacol 73:868-879, 2008), are concentrated in caveolae, underscoring their relevance to MOR G(s)alpha signaling. MOR-stimulated trafficking of G(s)alpha and AC into caveolae and the likelihood of increased MOR G(s)alpha coupling within caveolae could suggest that they contain the downstream effectors for MOR G(s)alpha AC signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.