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- W2924322293 endingPage "1441" @default.
- W2924322293 startingPage "1441" @default.
- W2924322293 abstract "Intracellular signaling mechanisms underlying the opioid system regulation of nociception, neurotransmitters release, stress responses, depression, and the modulation of reward circuitry have been investigated from different points of view. The presence of the ubiquitin proteasome system (UPS) in the synaptic terminations suggest a potential role of ubiquitin-dependent mechanisms in the control of the membrane occupancy by G protein-coupled receptors (GPCRs), including those belonging to the opioid family. In this review, we focused our attention on the role played by the ubiquitination processes and by UPS in the modulation of opioid receptor signaling and in pathological conditions involving the endogenous opioid system. The collective evidence here reported highlights the potential usefulness of proteasome inhibitors in neuropathic pain, addictive behavior, and analgesia since these molecules can reduce pain behavioral signs, heroin self-administration, and the development of morphine analgesic tolerance. Moreover, the complex mechanisms involved in the effects induced by opioid agonists binding to their receptors include the ubiquitination process as a post-translational modification which plays a relevant role in receptor trafficking and degradation. Hence, UPS modulation may offer novel opportunities to control the balance between therapeutic versus adverse effects evoked by opioid receptor activation, thus, representing a promising druggable target." @default.
- W2924322293 created "2019-04-01" @default.
- W2924322293 creator A5017229105 @default.
- W2924322293 creator A5025307452 @default.
- W2924322293 creator A5045961245 @default.
- W2924322293 creator A5058216130 @default.
- W2924322293 creator A5078562133 @default.
- W2924322293 date "2019-03-21" @default.
- W2924322293 modified "2023-10-14" @default.
- W2924322293 title "Interplay between the Endogenous Opioid System and Proteasome Complex: Beyond Signaling" @default.
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