Disruption of Abcg5 and Abcg8 in mice reveals their crucial role in biliary cholesterol secretion

By Liqing Yu, R. Hammer, J. Li-Hawkins, K. von Bergmann, D. Lutjohann, Jonathan C. Cohen, Helen H. Hobbs. Proceedings of the National Academy of Sciences of the United States of America, 2002

785 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Surgery

View Paper: https://www.semanticscholar.org/paper/afbd557ca60f68855123fbedc27de4fda8f95599

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Citations in the corpus

ABCG1 has a critical role in mediating cholesterol efflux to HDL and preventing cellular lipid accumulation. (2005, background): “, 2002) and accumulation of cholesterol (or oil red O staining) in the lungs, liver, and/or brain (McNeish et al., 2000; Wang et al., 2002; Yu et al., 2002).”
Liver X receptor signaling pathways in cardiovascular disease. (2003, neutral): “Initial studies postulated that ABCA1 may be the key target responsible for LXR inhibition of cholesterol absorption; however, recent studies suggest that ABCG5 and ABCG8 may play a more prominent role in this effect (32, 33).”
Xenobiotic, Bile Acid, and Cholesterol Transporters: Function and Regulation (2010, background): “In addition, biliary cholesterol levels are very low in Abcg5/g8-null mice (Yu et al., 2002).”
Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, positive): “Furthermore, LXR regulates the expression of cholesterol and lipid transporting proteins, such as ABCG5 and ABCG8 in the intestine or ABCG1, ABCA1 and apolipoproteins E and C in macrophages (Yu et al. 2002; Zelcer and Tontonoz 2006).”
Thematic review series: Brain Lipids. Cholesterol metabolism in the central nervous system during early development and in the mature animal Published, JLR Papers in Press, May 16, 2004. DOI 10.1194/jlr.R400004-JLR200 (2004, background): “half transporters that can move unesterified cholesterol from the cell membrane or cytosol to the external environment (39).”
Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. (2004, positive): “The decreases in the regulatory enzymes of both the classic and alternative pathways of bile acid synthesis as well as the decrease in ABCG5 and ABCG8 induced by LPS and cytokines suggest that during infection the body’s need to conserve cholesterol is so essential that all of these pathways are dow”
Cellular cholesterol trafficking and compartmentalization (2008, background): “Sterol entering the hepatocyte through SRB1 is shuttled to the canalicular membrane where it is secreted in an ABCG5/G8-transporter-dependent manner into the bil”