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By a genome-wide siRNA screen, we previously identified subunits of the Coat protein I (COPI) complex to limit LDL uptake into Huh-7 hepatocarcinoma cells.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>\n                    These findings were validated by targeted\n                    <jats:italic>in vitro<\/jats:italic>\n                    experiments as well as genetic association studies in humans and three mouse models with mutated or disrupted COPI genes.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    Silencing of\n                    <jats:italic>COPA<\/jats:italic>\n                    ,\n                    <jats:italic>COPB1<\/jats:italic>\n                    ,\n                    <jats:italic>COPB2<\/jats:italic>\n                    ,\n                    <jats:italic>ARCN1<\/jats:italic>\n                    ,\n                    <jats:italic>COPG1<\/jats:italic>\n                    , and\n                    <jats:italic>COPZ1<\/jats:italic>\n                    in Huh-7 cells resulted in decreased uptake of LDL and aberrant glycosylation and altered cell surface abundance of the LDL receptor (LDLR) as well as increased apoB secretion and cellular lipid storage. Single nucleotide polymorphisms of\n                    <jats:italic>ARCN1<\/jats:italic>\n                    were associated with lower ARCN1 expression and higher levels of LDL-cholesterol (LDL-C). Rare variants of\n                    <jats:italic>COPA<\/jats:italic>\n                    and\n                    <jats:italic>COPG1<\/jats:italic>\n                    were enriched among patients with LDL-C &gt; 5 mmol\/L. Patients and mice carrying other rare immunopathogenic missense variants of\n                    <jats:italic>COPA<\/jats:italic>\n                    and\n                    <jats:italic>COPG1<\/jats:italic>\n                    did not present with elevated plasma levels of LDL-C, while hepatic knockdown of murine\n                    <jats:italic>Copg1<\/jats:italic>\n                    increased the concentrations of non-HDL-cholesterol in plasma and triglycerides in the liver.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>The COPI coatomer regulates LDLR activity and apoB secretion as well as lipid content of liver cells. Loss of function of some variants of COPI genes are associated with higher LDL-C levels.<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.05.30.728950","type":"posted-content","created":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T17:55:13Z","timestamp":1780509313000},"source":"Crossref","is-referenced-by-count":1,"title":["The COPI coatomer influences LDL receptor activity, hepatic lipid storage, and apoB secretion"],"prefix":"10.64898","author":[{"given":"Grigorios","family":"Panteloglou","sequence":"first","affiliation":[{"name":"Institute for Clinical Chemistry, University of Zurich and University Hospital Zurich, Zurich, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00e9r\u00f4me","family":"Robert","sequence":"additional","affiliation":[{"name":"Institute for Clinical Chemistry, University of Zurich and University Hospital Zurich, Zurich, 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