Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9.
By S. Rashid, David E Curtis, R. Garuti, Norma N. Anderson, Y. Bashmakov, Y. K. Ho, R. Hammer, Y. Moon, Jay D. Horton. Proceedings of the National Academy of Sciences of the United States of America, 2005
725 citations recorded by the source corpus.
Subfields: Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/1c54a5407eac9f498ae0dec333584ef911f9cdf0
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
- Lisa N. Kinch
- Nick V. Grishin
- Robert Langer
- Daniel G. Anderson
- Helen H. Hobbs
- Jonathan C. Cohen
- M. Manoharan
- Jay D. Horton
In Surgery
- Jonathan C. Cohen
- Jay D. Horton
- Helen H. Hobbs
- M. Manoharan
- Robert Langer
- J. Goldstein
- Michael S. Brown
- V. Mohanraj
Citations in the corpus
- Molecular characterization of loss-of-function mutations in PCSK9 and identification of a compound heterozygote. (2006, background): “The normal fertility and development of the PCSK9knockout mice are consistent with this conclusion.(13) We cannot exclude the possibility that the mutant PCSK9 ex-”
- Therapeutic RNAi targeting PCSK9 acutely lowers plasma cholesterol in rodents and LDL cholesterol in nonhuman primates (2008, background): “Additional studies showed that the deletion of Pcsk9 in mice resulted in increased LDLR levels, accelerated the clearance of low density lipoprotein cholesterol (LDLc), and reduced circulating cholesterol levels (5).”
- Molecular biology of PCSK9: its role in LDL metabolism. (2007, background): “Therefore, inhibition of PCSK9 activity would be predicted to augment statin-induced LDLR expression and accelerate LDL-C clearance, as was observed when statins were administered to PCSK9 knockout mice [32].”