Control of cellular cholesterol efflux by the nuclear oxysterol receptor LXR alpha.

By Asha Venkateswaran, B. Laffitte, S. Joseph, P. A. Mak, Damien C. Wilpitz, P. Edwards, P. Tontonoz. Proceedings of the National Academy of Sciences of the United States of America, 2000

1,066 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Surgery

View Paper: https://www.semanticscholar.org/paper/327a2f31fa156bafd00b27dfc68af57595135a05

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. I. Tabas
2. P. Tontonoz
3. A. Calkin
4. S. Bensinger
5. N. Zelcer
6. Bart Staels
7. K. Bornfeldt
8. A. Lichtman

In Oncology

1. P. Tontonoz
2. S. Bensinger
3. N. Zelcer
4. P. Edwards
5. I. Tabas
6. A. Calkin

In Surgery

1. I. Tabas
2. P. Tontonoz
3. A. Calkin
4. S. Bensinger
5. N. Zelcer
6. J. Fruchart
7. P. Edwards
8. Bart Staels

Citations in the corpus

• Transcriptional integration of metabolism by the nuclear sterol-activated receptors LXR and FXR (2012, background): “ABCA1 was one of the earliest identified LXR target genes and is one of the most highly regulated LXR target”
• Apoptotic cells promote their own clearance and immune tolerance through activation of LXR (2009, positive): “7 cells ectopically expressing LXRa (Venkateswaran et al., 2000) (RAW-LXRa; Figure S6A).”
• ABCG1 has a critical role in mediating cholesterol efflux to HDL and preventing cellular lipid accumulation. (2005, methodology): “Peritoneal macrophages and lipid efflux assays Peritoneal macrophages were obtained from thioglycollate-treated mice as described (Venkateswaran et al., 2000).”
• Macrophage death and defective inflammation resolution in atherosclerosis (2009, background): “LXR activation is also involved in a key step in atherosclerosis regression, namely cholesterol efflux from cholesterol-loaded macrophage”
• Induction of phase I, II and III drug metabolism/transport by xenobiotics (2005, background): “…xenobiotics and a potential homeostatic cell survival response. enzymes in the body, and they range from endogenous compounds such as the steroids and cholesterol to drugs as well as potential carcinogens found in the environment (Lehmann et aL, 1997; Venkateswaran et aL, 2000; Wang et aL, 1999).”
• PPAR-α and PPAR-γ activators induce cholesterol removal from human macrophage foam cells through stimulation of the ABCA1 pathway (2001, background): “Since LXR-α has been shown to display constitutive activity in the absence of added exogenous ligand”