{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T21:33:39Z","timestamp":1790285619828,"version":"4.1.0"},"reference-count":27,"publisher":"Springer Science and Business Media LLC","issue":"1","content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["BMC Genomics"],"published-print":{"date-parts":[[2008,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>Selenoprotein S (SelS) protects the functional integrity of the endoplasmic reticulum against the deleterious effects of metabolic stress. <jats:italic>SEPS1\/SelS<\/jats:italic> polymorphisms have been involved in the increased release of pro-inflammatory cytokines interleukin (IL)-1\u03b2, tumor necrosis factor (TNF)-\u03b1 and IL-6 in macrophages. We aimed at investigating the role of the <jats:italic>SEPS1<\/jats:italic> variants previously associated with higher plasma levels of these cytokines and of the <jats:italic>SEPS1<\/jats:italic> haplotypes in the susceptibility to develop immune-mediated diseases characterized by an inflammatory component.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Six polymorphisms distributed through the <jats:italic>SEPS1<\/jats:italic> gene (rs11327127, rs28665122, rs4965814, rs12917258, rs4965373 and rs2101171) were genotyped in more than two thousand patients suffering from type 1 diabetes, rheumatoid arthritis or inflammatory bowel diseases and 550 healthy controls included in the case-control study.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>Lack of association of <jats:italic>SEPS1<\/jats:italic> polymorphisms or haplotypes precludes a major role of this gene increasing predisposition to these inflammatory diseases.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1471-2164-9-329","type":"journal-article","created":{"date-parts":[[2008,7,15]],"date-time":"2008-07-15T06:13:45Z","timestamp":1216102425000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["Polymorphisms in the selenoprotein S gene: lack of association with autoimmune inflammatory diseases"],"prefix":"10.1186","volume":"9","author":[{"given":"Alfonso","family":"Mart\u00ednez","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jose Luis","family":"Santiago","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jezabel","family":"Varad\u00e9","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana","family":"M\u00e1rquez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos\u00e9 Ram\u00f3n","family":"Lamas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan Luis","family":"Mendoza","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hermenegildo","family":"de la Calle","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuel","family":"D\u00edaz-Rubio","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emilio G","family":"de la Concha","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjam\u00edn","family":"Fern\u00e1ndez-Guti\u00e9rrez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Urcelay","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2008,7,14]]},"reference":[{"key":"1522_CR1","doi-asserted-by":"publisher","first-page":"841","DOI":"10.1038\/nature02656","volume":"429","author":"Y Ye","year":"2004","unstructured":"Ye Y, Shibata Y, Yun C, Ron D, Rapoport TA: A membrane protein complex mediates retro-translocation from the ER lumen into the cytosol. 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