ArticleDisease models & mechanisms2014
Loss of lysosomal membrane protein NCU-G1 in mice results in spontaneous liver fibrosis with accumulation of lipofuscin and iron in Kupffer cells.
Article in Disease models & mechanisms, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Fas apoptotic inhibitor molecule 2 mitigates metabolic dysfunction-associated fatty liver disease through autophagic CRTC2 degradation.Experimental & molecular medicine · 2025Article
- Glycosylated lysosomal membrane protein promotes tissue repair after spinal cord injury by reducing iron deposition and ferroptosis in microglia.Scientific reports · 2025Article
- Cathepsin D is essential for the degradomic shift of macrophages required to resolve liver fibrosis.Molecular metabolism · 2024Article
- Essential role of MFSD1-GLMP-GIMAP5 in lymphocyte survival and liver homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- [Lysosomal membrane proteinNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Article
- Chick fetal organ spheroids as a model to study development and disease.BMC molecular and cell biology · 2021Article
- Common Transcriptional Program of Liver Fibrosis in Mouse Genetic Models and Humans.International journal of molecular sciences · 2021Article
- Article
- Ferritinophagy drives uropathogenic Escherichia coli persistence in bladder epithelial cells.Autophagy · 2016Article
- Age-dependent development of liver fibrosis in Glmp (gt/gt) mice.Fibrogenesis & tissue repair · 2016Article
- Lack of the Lysosomal Membrane Protein, GLMP, in Mice Results in Metabolic Dysregulation in Liver.PloS one · 2015Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human kidney predominant protein, NCU-G1, is a highly conserved protein with an unknown biological function. Initially described as a nuclear protein, it was later 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-g1(gt/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 an increased rate of hepatic cell death, oxidative stress and active fibrogenesis were detected in Ncu-g1(gt/gt) liver. In addition to collagen deposition, microscopic examination of liver sections revealed accumulation of autofluorescent lipofuscin and iron in Ncu-g1(gt/gt) Kupffer cells. Because only a few transgenic mouse models have been identified with chronic liver injury and spontaneous liver fibrosis development, we propose that the Ncu-g1(gt/gt) mouse could be a valuable new tool in the development of novel treatments for the attenuation of fibrosis due to chronic liver damage.
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