{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T02:57:36Z","timestamp":1790650656479,"version":"4.1.0"},"reference-count":33,"publisher":"National Academy of Sciences","issue":"19","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2011,5,10]]},"abstract":"<jats:p>\n                    Transporters at the hepatic canalicular membrane are essential for the formation of bile and the prevention of cholestatic liver disease. One such example is ATP8B1, a P4-type ATPase disrupted in three inherited forms of intrahepatic cholestasis. Mutation of the X-linked mouse gene\n                    <jats:italic>Atp11c<\/jats:italic>\n                    , which encodes a paralogous P4-type ATPase, precludes B-cell development in the adult bone marrow, but also causes hyperbilirubinemia. Here we explore this hyperbilirubinemia in two independent\n                    <jats:italic>Atp11c<\/jats:italic>\n                    mutant mouse lines, and find that it originates from an effect on nonhematopoietic cells. Liver function tests and histology revealed only minor pathology, although cholic acid was elevated in the serum of mutant mice, and became toxic to mutant mice when given as a dietary supplement. The majority of homozygous mutant females also died of dystocia in a maternal genotype-specific manner. ATP11C therefore represents a multifunctional transporter, essential for adult B-cell development, the prevention of intrahepatic cholestasis, and parturition, and is a new candidate for genetically undiagnosed cases of cholestasis and dystocia in humans.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1104631108","type":"journal-article","created":{"date-parts":[[2011,4,25]],"date-time":"2011-04-25T23:05:55Z","timestamp":1303772755000},"page":"7890-7895","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":63,"title":["X-linked cholestasis in mouse due to mutations of the P4-ATPase ATP11C"],"prefix":"10.1073","volume":"108","author":[{"given":"Owen M.","family":"Siggs","sequence":"first","affiliation":[{"name":"Department of Genetics and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernd","family":"Schnabl","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California at San Diego, School of Medicine, La Jolla, CA 92093"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bill","family":"Webb","sequence":"additional","affiliation":[{"name":"Center for Metabolomics and Mass Spectrometry, The Scripps Research Institute, La Jolla, CA 92037; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce","family":"Beutler","sequence":"additional","affiliation":[{"name":"Department of Genetics and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2011,4,25]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.72.121801.161712"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199810223391707"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/ng0398-219"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1053\/jhep.2001.27663"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/3034"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(99)70287-8"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.1.282"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90446-4"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90380-9"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1591"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbalip.2009.02.008"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni.2012"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni.2011"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2008.10.017"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2008.03.002"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI34138"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddh100"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature01339"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)00062-3"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1021\/mp060009t"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.98.4.2011"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.hep.2003.09.037"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2008.07.065"},{"key":"e_1_3_3_24_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm1501"},{"key":"e_1_3_3_25_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.71.102301.093055"},{"key":"e_1_3_3_26_2","doi-asserted-by":"publisher","DOI":"10.3748\/wjg.15.2049"},{"key":"e_1_3_3_27_2","first-page":"1237","article-title":"Mice with homozygous disruption of the mdr2 P-glycoprotein gene. 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