{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T03:08:53Z","timestamp":1791342533122,"version":"4.3.1"},"reference-count":27,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2014,6,27]],"date-time":"2014-06-27T00:00:00Z","timestamp":1403827200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004794","name":"Centre National pour la Recherche Scientifique","doi-asserted-by":"crossref","award":["R06048AA"],"award-info":[{"award-number":["R06048AA"]}],"id":[{"id":"10.13039\/501100004794","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100002915","name":"Fondation pour la Recherche M\u00e9dicale","doi-asserted-by":"crossref","award":["R09070AA"],"award-info":[{"award-number":["R09070AA"]}],"id":[{"id":"10.13039\/501100002915","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000890","name":"National Multiple Sclerosis Society","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100000890","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The tetrodotoxin\u2010resistant (<jats:styled-content style=\"fixed-case\">TTX<\/jats:styled-content>\u2010R) voltage\u2010gated sodium channel Na<jats:sub>v<\/jats:sub>1.8 is predominantly expressed in peripheral afferent neurons, but in case of neuronal injury an ectopic and detrimental expression of Na<jats:sub>v<\/jats:sub>1.8 occurs in neurons of the <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content>. In <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> neurons, Na<jats:sub>v<\/jats:sub>1.2 and Na<jats:sub>v<\/jats:sub>1.6 channels accumulate at the axon initial segment, the site of the generation of the action potential, through a direct interaction with the scaffolding protein ankyrin G (ankG). This interaction is regulated by protein kinase <jats:styled-content style=\"fixed-case\">CK<\/jats:styled-content>2 phosphorylation. In this study, we quantitatively analyzed the interaction between Na<jats:sub>v<\/jats:sub>1.8 and ankG. <jats:styled-content style=\"fixed-case\">GST<\/jats:styled-content> pull\u2010down assay and surface plasmon resonance technology revealed that Na<jats:sub>v<\/jats:sub>1.8 strongly and constitutively interacts with ankG, in comparison to what observed for Na<jats:sub>v<\/jats:sub>1.2. An ion channel bearing the ankyrin\u2010binding motif of Na<jats:sub>v<\/jats:sub>1.8 displaced the endogenous Na<jats:sub>v<\/jats:sub>1 accumulation at the axon initial segment of hippocampal neurons. Finally, Na<jats:sub>v<\/jats:sub>1.8 and ankG co\u2010localized in skin nerves fibers. Altogether, these results indicate that Na<jats:sub>v<\/jats:sub>1.8 carries all the information required for its localization at ankG micro\u2010domains. The constitutive binding of Na<jats:sub>v<\/jats:sub>1.8 with ankG could contribute to the pathological aspects of illnesses where Na<jats:sub>v<\/jats:sub>1.8 is ectopically expressed in <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> neurons.<\/jats:p><jats:p>\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc12785-fig-0005-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text>\nThe peripheral voltage\u2010gated sodium channel Na<jats:sub>v<\/jats:sub>1.8 can be abnormally expressed in central nervous system (CNS) neurons in cases of neuronal injury. We here demonstrated that Na<jats:sub>v<\/jats:sub>1.8 binds strongly and constitutively to the scaffolding protein ankyrin G. This indicates that Na<jats:sub>v<\/jats:sub>1.8 concentrates at the ankyrin G micro\u2010domains and could disturb the electrophysiological signature of CNS neurons where it is ectopicaly expressed.\n<\/jats:p>","DOI":"10.1111\/jnc.12785","type":"journal-article","created":{"date-parts":[[2014,6,5]],"date-time":"2014-06-05T16:13:13Z","timestamp":1401984793000},"page":"33-41","source":"Crossref","is-referenced-by-count":14,"title":["Tetrodotoxin\u2010resistant voltage\u2010gated sodium channel Na<sub>v<\/sub>1.8 constitutively interacts with ankyrin G"],"prefix":"10.1111","volume":"131","author":[{"given":"Audrey","family":"Montersino","sequence":"first","affiliation":[{"name":"Aix Marseille Universit\u00e9 CNRS CRN2M\u2010UMR7286 Marseille France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Brachet","sequence":"additional","affiliation":[{"name":"Aix Marseille Universit\u00e9 CNRS CRN2M\u2010UMR7286 Marseille 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