{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T20:28:22Z","timestamp":1772137702898,"version":"3.50.1"},"reference-count":22,"publisher":"Rockefeller University Press","issue":"6","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2005,3,14]]},"abstract":"<jats:p>A glutamic acid deletion (\u0394E) in the AAA+ protein torsinA causes DYT1 dystonia. Although the majority of torsinA resides within the endoplasmic reticulum (ER), torsinA binds a substrate in the lumen of the nuclear envelope (NE), and the \u0394E mutation enhances this interaction. Using a novel cell-based screen, we identify lamina-associated polypeptide 1 (LAP1) as a torsinA-interacting protein. LAP1 may be a torsinA substrate, as expression of the isolated lumenal domain of LAP1 inhibits the NE localization of \u201csubstrate trap\u201d EQ-torsinA and EQ-torsinA coimmunoprecipitates with LAP1 to a greater extent than wild-type torsinA. Furthermore, we identify a novel transmembrane protein, lumenal domain like LAP1 (LULL1), which also appears to interact with torsinA. Interestingly, LULL1 resides in the main ER. Consequently, torsinA interacts directly or indirectly with a novel class of transmembrane proteins that are localized in different subdomains of the ER system, either or both of which may play a role in the pathogenesis of DYT1 dystonia.<\/jats:p>","DOI":"10.1083\/jcb.200411026","type":"journal-article","created":{"date-parts":[[2005,3,14]],"date-time":"2005-03-14T21:41:59Z","timestamp":1110836519000},"page":"855-862","update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":204,"title":["The AAA+ protein torsinA interacts with a conserved domain present in LAP1 and a novel ER protein"],"prefix":"10.1083","volume":"168","author":[{"given":"Rose E.","family":"Goodchild","sequence":"first","affiliation":[{"name":"1Department of Neurology, Columbia University, New York, NY 10032"}]},{"given":"William T.","family":"Dauer","sequence":"additional","affiliation":[{"name":"1Department of Neurology, Columbia University, New York, NY 10032"},{"name":"2Department of Pharmacology, Columbia University, New York, NY 10032"}]}],"member":"291","published-online":{"date-parts":[[2005,3,14]]},"reference":[{"key":"2023072906465795900_BIB1","doi-asserted-by":"crossref","first-page":"1195","DOI":"10.1093\/brain\/121.7.1195","volume":"121","year":"1998","journal-title":"Brain."},{"key":"2023072906465795900_BIB2","doi-asserted-by":"crossref","first-page":"575","DOI":"10.1038\/nrm879","volume":"3","year":"2002","journal-title":"Nat. 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