ArticleWorld journal of gastroenterology2007
Overexpression of the cholesterol-binding protein MLN64 induces liver damage in the mouse.
Article in World journal of gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Exploring the lutein therapeutic potential in steatotic liver disease: mechanistic insights and future directions.Frontiers in pharmacology · 2024Review
- Review
- Targeting the lysosome: Mechanisms and treatments for nonalcoholic fatty liver disease.Journal of cellular biochemistry · 2022Review
- MLN64 induces mitochondrial dysfunction associated with increased mitochondrial cholesterol content.Redox biology · 2017Article
- ER-endosome contact sites: molecular compositions and functions.The EMBO journal · 2015Review
- HDAC8-mediated epigenetic reprogramming plays a key role in resistance to anthrax lethal toxin-induced pyroptosis in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Cellular adaptation to anthrax lethal toxin-induced mitochondrial cholesterol enrichment, hyperpolarization, and reactive oxygen species generation through downregulating MLN64 in macrophages.Molecular and cellular biology · 2012Article
- STARTing to understand MLN64 function in cholesterol transport.Journal of lipid research · 2010Article
- Overexpression of STARD3 in human monocyte/macrophages induces an anti-atherogenic lipid phenotype.Clinical science (London, England : 1979) · 2010Article
- Inter-organelle ER-endolysosomal contact sites in metabolism and disease across evolution.Communicative & integrative biologyReview
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo examine the in vivo phenotype associated with hepatic metastatic lymph node 64 (MLN64) over-expression.
methodsRecombinant-adenovirus-mediated MLN64 gene transfer was used to overexpress MLN64 in the livers of C57BL/6 mice. We measured the effects of MLN64 overexpression on hepatic cholesterol content, bile flow, biliary lipid secretion and apoptosis markers. For in vitro studies cultured CHO cells with transient MLN64 overexpression were utilized and apoptosis by TUNEL assay was measured.
resultsLivers from Ad.MLN64-infected mice exhibited early onset of liver damage and apoptosis. This response correlated with increases in liver cholesterol content and biliary bile acid concentration, and impaired bile flow. We investigated whether liver MLN64 expression could be modulated in a murine model of hepatic injury. We found increased hepatic MLN64 mRNA and protein levels in mice with chenodeoxycholic acid-induced liver damage. In addition, cultured CHO cells with transient MLN64 overexpression showed increased apoptosis.
conclusionIn summary, hepatic MLN64 over-expression induced damage and apoptosis in murine livers and altered cholesterol metabolism. Further studies are required to elucidate the relevance of these findings under physiologic and disease conditions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.