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Voltage-gated sodium channel Na\n                  <jats:sub>V<\/jats:sub>\n                  1.8, a pivotal driver of pain signaling, is a clinically validated target for the development of novel, non-addictive pain therapeutics. Small molecule inhibitors against Na\n                  <jats:sub>V<\/jats:sub>\n                  1.8 have shown promise in acute pain indications, but large clinical effect sizes have not yet been demonstrated and efficacy in chronic pain indications are lacking.\n                <\/jats:p>\n                <jats:p>\n                  An alternative strategy to target Na\n                  <jats:sub>V<\/jats:sub>\n                  1.8 channels for analgesia is to reduce the number of channels that are present on nociceptor membranes. We generated a therapeutic heterobifunctional protein, named UbiquiNa\n                  <jats:sub>V<\/jats:sub>\n                  , that contains a Na\n                  <jats:sub>V<\/jats:sub>\n                  1.8-selective binding module and the catalytic subunit of the NEDD4 E3 Ubiquitin ligase. We show that UbiquiNav significantly reduces channel expression in the plasma membrane and reduces Na\n                  <jats:sub>V<\/jats:sub>\n                  1.8 currents in rodent sensory neurons. We demonstrate that UbiquiNa\n                  <jats:sub>V<\/jats:sub>\n                  is selective for Na\n                  <jats:sub>V<\/jats:sub>\n                  1.8 over other Na\n                  <jats:sub>V<\/jats:sub>\n                  isoforms and other components of the sensory neuronal electrogenisome. We then show that UbiquiNa\n                  <jats:sub>V<\/jats:sub>\n                  normalizes the distribution of Na\n                  <jats:sub>V<\/jats:sub>\n                  1.8 protein to distal axons, and that UbiquiNa\n                  <jats:sub>V<\/jats:sub>\n                  normalizes the neuronal hyperexcitability in\n                  <jats:italic>in vitro<\/jats:italic>\n                  models of inflammatory and chemotherapy-induced neuropathic pain. Our results serve as a blueprint for the design of therapeutics that leverage the selective ubiquitination of Na\n                  <jats:sub>V<\/jats:sub>\n                  1.8 channels for analgesia.\n                <\/jats:p>","DOI":"10.1101\/2025.02.04.636451","type":"posted-content","created":{"date-parts":[[2025,2,4]],"date-time":"2025-02-04T20:40:42Z","timestamp":1738701642000},"source":"Crossref","is-referenced-by-count":7,"title":["Targeted ubiquitination of Na\n                  <sub>V<\/sub>\n                  1.8 reduces sensory neuronal excitability"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6097-0541","authenticated-orcid":false,"given":"Sidharth","family":"Tyagi","sequence":"first","affiliation":[{"name":"Medical Scientist Training Program, Yale School of Medicine, New Haven, CT, USA"},{"name":"Center for Neuroscience and Regeneration Research, West Haven, CT, USA"},{"name":"Department of Neurology, Yale School of Medicine, New Haven, CT, 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