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We previously cloned a NAT (\n                    <jats:italic>Nat9a)<\/jats:italic>\n                    to\n                    <jats:italic>Scn9a<\/jats:italic>\n                    , which encodes the Na\n                    <jats:sub>V<\/jats:sub>\n                    1.7 voltage-gated sodium channel that is essential for pain perception. By studying a novel\n                    <jats:italic>Nat9a<\/jats:italic>\n                    global knockout mouse model, we demonstrate that the deletion of\n                    <jats:italic>Nat9a<\/jats:italic>\n                    does not affect pain sensitivity but instead partially impairs motor coordination. We show that\n                    <jats:italic>Nat9a<\/jats:italic>\n                    is expressed throughout the peripheral and central nervous systems and its expression is enriched, but not limited to, cells that express parvalbumin (\n                    <jats:italic>Pvalb),<\/jats:italic>\n                    which is a marker for proprioceptors in DRG and a subclass of interneurons in spinal cord and brain.\n                    <jats:italic>Nat9a<\/jats:italic>\n                    knockout leads to an increase in\n                    <jats:italic>Scn9a<\/jats:italic>\n                    expression, confirming\n                    <jats:italic>Nat9a<\/jats:italic>\n                    \u2019s physiological role as a negative regulator of\n                    <jats:italic>Scn9a<\/jats:italic>\n                    . Furthermore, CRISPR activation of\n                    <jats:italic>Nat9a<\/jats:italic>\n                    transcription in Cad cells suppresses endogenous\n                    <jats:italic>Scn9a<\/jats:italic>\n                    expression. Notably\n                    <jats:italic>Nat9a<\/jats:italic>\n                    expression in\n                    <jats:italic>Pvalb<\/jats:italic>\n                    \u2009+\u2009neurons coincides with that of the\n                    <jats:italic>Scn1a<\/jats:italic>\n                    gene (Na\n                    <jats:sub>V<\/jats:sub>\n                    1.1 sodium channel) with both genes sharing a divergent bi-part promoter region. This suggests a mechanism by which\n                    <jats:italic>Nat9a<\/jats:italic>\n                    transcription leads to suppression of\n                    <jats:italic>Scn9a<\/jats:italic>\n                    and promotes neuronal expression of Na\n                    <jats:sub>V<\/jats:sub>\n                    1.1 over Na\n                    <jats:sub>V<\/jats:sub>\n                    1.7.\n                  <\/jats:p>","DOI":"10.1038\/s41598-026-48500-8","type":"journal-article","created":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T14:57:22Z","timestamp":1776351442000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Natural antisense transcript Nat9a suppresses Scn9a (NaV1.7) expression in parvalbumin-positive proprioceptive and inhibitory neurons"],"prefix":"10.1038","volume":"16","author":[{"given":"Shengnan","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sonia","family":"Santana-Varela","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hajar","family":"Mikaeili","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abdella M.","family":"Habib","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janvi","family":"Patel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naxi","family":"Tian","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrei L.","family":"Okorokov","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James J.","family":"Cox","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,4,16]]},"reference":[{"key":"48500_CR1","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2458-11-770","volume":"11","author":"DS Goldberg","year":"2011","unstructured":"Goldberg, D. 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