ArticleProceedings of the National Academy of Sciences of the United States of America2001
Chronic morphine induces the concomitant phosphorylation and altered association of multiple signaling proteins: a novel mechanism for modulating cell signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 67 citations in OpenAlex.
- Relevance of Mu-Opioid Receptor Splice Variants and Plasticity of Their Signaling Sequelae to Opioid Analgesic Tolerance.Cellular and molecular neurobiology · 2021Review
- Phosphorylation of unique C-terminal sites of the mu-opioid receptor variants 1B2 and 1C1 influences their Gs association following chronic morphine.Journal of neurochemistry · 2020Article
- Acute ethanol exposure reduces serotonin receptor 1A internalization by increasing ubiquitination and degradation of β-arrestin2.The Journal of biological chemistry · 2019Article
- Dynamic Opioid Receptor Regulation in the Periphery.Molecular pharmacology · 2019Review
- Decrease of inhibitory synaptic currents of locus coeruleus neurons via orexin type 1 receptors in the context of naloxone-induced morphine withdrawal.The journal of physiological sciences : JPS · 2019Article
- G protein subunit phosphorylation as a regulatory mechanism in heterotrimeric G protein signaling in mammals, yeast, and plants.The Biochemical journal · 2018Review
- Acute morphine alters GABAergic transmission in the central amygdala during naloxone-precipitated morphine withdrawal: role of cyclic AMP.Frontiers in integrative neuroscience · 2014Article
- A novel noncanonical signaling pathway for the μ-opioid receptor.Molecular pharmacology · 2013Article
- Opioid receptor trafficking and signaling: what happens after opioid receptor activation?Cellular and molecular neurobiology · 2012Review
- Pleiotropic opioid regulation of spinal endomorphin 2 release and its adaptations to opioid withdrawal are sexually dimorphic.The Journal of pharmacology and experimental therapeutics · 2012Article
- Article
- Down-regulation of c-Cbl by morphine accounts for persistent ERK1/2 signaling in delta-opioid receptor-expressing HEK293 cells.The Journal of biological chemistry · 2009Article
- Mu-opioid receptor redistribution in the locus coeruleus upon precipitation of withdrawal in opiate-dependent rats.Anatomical record (Hoboken, N.J. : 2007) · 2009Article
- Src phosphorylation of micro-receptor is responsible for the receptor switching from an inhibitory to a stimulatory signal.The Journal of biological chemistry · 2009Article
- Physiological roles for G protein-regulated adenylyl cyclase isoforms: insights from knockout and overexpression studies.Neuro-Signals · 2009Review
- Oxycodone plus ultra-low-dose naltrexone attenuates neuropathic pain and associated mu-opioid receptor-Gs coupling.The journal of pain · 2008Article
- Augmentation of spinal morphine analgesia and inhibition of tolerance by low doses of mu- and delta-opioid receptor antagonists.British journal of pharmacology · 2007Article
- Engineered G protein coupled receptors reveal independent regulation of internalization, desensitization and acute signaling.BMC biology · 2005Article
- Reciprocal modulation of phospholipase Cbeta isoforms: adaptation to chronic morphine.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Chronic morphine treatment inhibits opioid receptor desensitization and internalization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traditional mechanisms thought to underlie opioid tolerance include receptor phosphorylation/down-regulation, G-protein uncoupling, and adenylyl cyclase superactivation. A parallel line of investigation also indicates that opioid tolerance development results from a switch from predominantly opioid receptor G(i alpha) inhibitory to G(beta gamma) stimulatory signaling. As described previously, this results, in part, from the increased relative abundance of G(beta gamma)-stimulated adenylyl cyclase isoforms as well as from a profound increase in their phosphorylation [Chakrabarti, S., Rivera, M., Yan, S.-Z., Tang, W.-J. & Gintzler, A. R. (1998) Mol. Pharmacol. 54, 655-662; Chakrabarti, S., Wang, L., Tang, W.-J. & Gintzler, A. R. (1998) Mol. Pharmacol. 54, 949--953]. The present study demonstrates that chronic morphine administration results in the concomitant phosphorylation of three key signaling proteins, G protein receptor kinase (GRK) 2/3, beta-arrestin, and G(beta), in the guinea pig longitudinal muscle myenteric plexus tissue. Augmented phosphorylation of all three proteins is evident in immunoprecipitate obtained by using either anti-GRK2/3 or G(beta) antibodies, but the phosphorylation increment is greater in immunoprecipitate obtained with G(beta) antibodies. Analyses of coimmunoprecipitated proteins indicate that phosphorylation of GRK2/3, beta-arrestin, and G(beta) has varying consequences on their ability to associate. As a result, increased availability of and signaling via G(beta gamma) could occur without compromising the membrane content (and presumably activity) of GRK2/3. Induction of the concomitant phosphorylation of multiple proteins in a multimolecular complex with attendant modulation of their association represents a novel mechanism for increasing G(beta gamma) signaling and opioid tolerance formation.
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