ABCG1 has a critical role in mediating cholesterol efflux to HDL and preventing cellular lipid accumulation.
By M. Kennedy, G. Barrera, Kotoka Nakamura, Á. Baldán, Paul T. Tarr, M. Fishbein, J. Frank, O. Francone, P. Edwards. Cell Metabolism, 2005
911 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Surgery
View Paper: https://www.semanticscholar.org/paper/b0761ae7239287b1757134163fc9a78e0ae32826
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Citations in the corpus
- Apoptotic cells promote their own clearance and immune tolerance through activation of LXR (2009, neutral): “C57Bl/6 Abcg1 / and Sv129/C57Bl/6 Abca1 / mice and their WT controls have been described previously (Kennedy et al., 2005; Timmins et al., 2005).”
- LXR signaling couples sterol metabolism to proliferation in the acquired immune response (2008, background): “ABCG1 is known to play an important role in cholesterol and oxysterol efflux (Kennedy et al., 2005; Terasaka et al., 2007; Wang et al., 2004).”
- Macrophage ABCA1 and ABCG1, but not SR-BI, promote macrophage reverse cholesterol transport in vivo. (2007, background): “Mice lacking ABCG1 have evidence of lipid accumulation in certain tissue macrophages (14, 16), but the mechanism of this has not been proven to be impaired cholesterol efflux and RCT in vivo.”
- Molecular basis of cholesterol efflux via ABCG subfamily transporters (2021, background): “Subsequently, genetic manipulation studies in mice indicated that ABCG1 (G1) also transports cholesterol (8).”
- Transcriptional integration of metabolism by the nuclear sterol-activated receptors LXR and FXR (2012, background): “ABCG1 promotes cholesterol efflux to HDL, and it is likely that ABCA1 and ABCG1 act in concert to promote cholesterol removal in physiological contexts via HD”
- Functionally Defective High-Density Lipoprotein: A New Therapeutic Target at the Crossroads of Dyslipidemia, Inflammation, and Atherosclerosis (2006, background): “In addition to ABCA1, there are several other sterolregulated ABC transporters, including ABCG1 and ABCG4, which are involved in cholesterol efflux from macrophages to mature HDL2 and HDL3 particles (Nakamura et al., 2004; Wang et al., 2004; Kennedy et al., 2005).”