{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T22:17:12Z","timestamp":1789942632260,"version":"4.0.1"},"reference-count":81,"publisher":"The Company of Biologists","license":[{"start":{"date-parts":[[2021,5,18]],"date-time":"2021-05-18T00:00:00Z","timestamp":1621296000000},"content-version":"am","delay-in-days":2694,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Human kidney predominant protein, NCU-G1, is a highly conserved protein with an unknown biological function. Initially described as a nuclear protein, it has later been shown to be a bona fide lysosomal integral membrane protein. To gain insight into the physiological function of NCU-G1, mice with no detectable expression of this gene were created using a gene-trap strategy, and Ncu-g1gt\/gt mice were successfully characterized. Lysosomal disorders are mainly caused by lack of or malfunctioning of proteins in the endosomal-lysosomal pathway. The clinical symptoms vary, but often include liver dysfunction. Persistent liver damage activates fibrogenesis and if unremedied eventually leads to liver fibrosis\/cirrhosis and death. We demonstrate that the disruption of Ncu-g1 results in spontaneous liver fibrosis in mice as the predominant phenotype. Evidence for increased rate of hepatic cell death, oxidative stress and active fibrogenesis were detected in Ncu-g1gt\/gt liver. In addition to collagen deposition, microscopic examination of liver sections revealed accumulation of autofluorescent lipofuscin and iron in Ncu-g1gt\/gt Kupffer cells. As only a few transgenic mouse models have been identified with chronic liver injury and spontaneous liver fibrosis development, we propose that the Ncu-g1gt\/gt mouse may be a valuable new tool in the development of novel treatments for attenuation of fibrosis due to chronic liver damage.<\/jats:p>","DOI":"10.1242\/dmm.014050","type":"journal-article","created":{"date-parts":[[2014,1,31]],"date-time":"2014-01-31T03:48:56Z","timestamp":1391140136000},"source":"Crossref","is-referenced-by-count":11,"title":["Loss of lysosomal protein NCU-G1 results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells"],"prefix":"10.1242","author":[{"given":"Xiang Yi","family":"Kong","sequence":"first","affiliation":[{"name":"University of Oslo, Oslo, Norway;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cecilie K.","family":"Nesset","sequence":"additional","affiliation":[{"name":"University of Oslo, Oslo, Norway;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Damme","sequence":"additional","affiliation":[{"name":"Christian-Albrechts-Universit\u00e4t Kiel, Kiel, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Else-Marit","family":"L\u00f8berg","sequence":"additional","affiliation":[{"name":"Oslo University Hospital Ullevaal, Norway;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Torben","family":"L\u00fcbke","sequence":"additional","affiliation":[{"name":"Bielefeld University, Bielefeld, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"M\u00e6hlen","sequence":"additional","affiliation":[{"name":"Oslo University Hospital Ullevaal, Norway;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristin B.","family":"Andersson","sequence":"additional","affiliation":[{"name":"Oslo University Hospital Ullevaal, Norway;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petra I.","family":"Lorenzo","sequence":"additional","affiliation":[{"name":"University of Oslo, Oslo, Norway;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Norbert","family":"Roos","sequence":"additional","affiliation":[{"name":"University of Oslo, Oslo, Norway;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G. 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