ArticleMolecular pharmacology2008
Beta-arrestin-dependent mu-opioid receptor-activated extracellular signal-regulated kinases (ERKs) Translocate to Nucleus in Contrast to G protein-dependent ERK activation.
Article in Molecular pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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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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Who cites it
85 citing papers in PubMed, 155 citations in OpenAlex.
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- GPR17 modulates anxiety-like behaviorsActa pharmaceutica Sinica. B · 2024Article
- Ketamine and Major Ketamine Metabolites Function as Allosteric Modulators of Opioid Receptors.Molecular pharmacology · 2024Article
- GPCR kinases differentially modulate biased signaling downstream of CXCR3 depending on their subcellular localization.Science signaling · 2024Article
- Opioid Mechanisms and the Treatment of Depression.Current topics in behavioral neurosciences · 2024Review
- Diversity and specificity in location-based signaling outputs of neuronal GPCRs.Current opinion in neurobiology · 2022Review
- Opioid receptors signaling network.Journal of cell communication and signaling · 2022Article
- The opioid system in depression.Neuroscience and biobehavioral reviews · 2022Review
- Scaffolding of Mitogen-Activated Protein Kinase Signaling by β-Arrestins.International journal of molecular sciences · 2022Review
- Oxycodone in the Opioid Epidemic: High 'Liking', 'Wanting', and Abuse Liability.Cellular and molecular neurobiology · 2021Review
- Ketamine: A tale of two enantiomers.Journal of psychopharmacology (Oxford, England) · 2021Review
- Opioids Cause Sex-Specific Vascular Changes via Cofilin-Extracellular Signal-Regulated Kinase Signaling: Female Mice Present Higher Risk of Developing Morphine-Induced Vascular Dysfunction than Male Mice.Journal of vascular research · 2021Article
- Review
- β-Arrestin 2 and ERK1/2 Are Important Mediators Engaged in Close Cooperation between TRPV1 and µ-Opioid Receptors in the Plasma Membrane.International journal of molecular sciences · 2020Article
- NovelACS medicinal chemistry letters · 2020Article
- Signaling characteristics and functional regulation of delta opioid-kappa opioid receptor (DOP-KOP) heteromers in peripheral sensory neurons.Neuropharmacology · 2019Article
- Molecular dynamics of fentanyl bound to μ-opioid receptor.Journal of molecular modeling · 2019Article
- Mitogen-activated protein kinase signaling mediates opioid-induced presynaptic NMDA receptor activation and analgesic tolerance.Journal of neurochemistry · 2019Article
- Morphine regulates adult neurogenesis and contextual memory extinction via the PKCε/Prox1 pathway.Neuropharmacology · 2018Article
- Novel Roles of Non-Coding RNAs in Opioid Signaling and Cardioprotection.Non-coding RNA · 2018Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The cellular location of extracellular signal-regulated kinases (ERKs) activated by a G protein-coupled receptor was shown to be dependent on the pathway that mediated their activation. In general, fast activation of ERKs (2 min) mediated by G proteins resulted in the nuclear translocation of phosphorylated ERKs, whereas a slower activation of ERKs (10 min) mediated by beta-arrestins resulted in the cytosolic retention of the phosphorylated ERKs. However, we observed distinct differences from this established ERKs cellular itinerary with the mu-opioid receptor-activated ERKs. Agonists such as morphine and methadone activated ERKs via the protein kinase C-dependent pathway but not the beta-arrestin-dependent pathway. The activated ERKs did not translocate into the nucleus, but phosphorylated 90-kDa ribosomal S6 kinase and induced the activity of transcription factor cAMP response element-binding protein. In contrast, agonists such as etorphine and fentanyl activated ERKs in a beta-arrestin-dependent manner. The phosphorylated ERKs translocated into the nucleus, resulting in increases in Elk-1 activity and GRK2 and beta-arrestin2 transcriptions. Thus, the cellular location of phosphorylated ERKs and subsequent activities on gene transcriptions are dictated by the agonist used to activate the receptor and the subsequent signaling pathway involved.
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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.