Molecular biology of PCSK9: its role in LDL metabolism.
By Jay D. Horton, Jonathan C. Cohen, Helen H. Hobbs. TIBS -Trends in Biochemical Sciences. Regular ed, 2007
613 citations recorded by the source corpus.
Subfields: Cancer Research, Computational Theory and Mathematics, Surgery
View Paper: https://www.semanticscholar.org/paper/948934df70f941ac8c28dd903cb6926533069957
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- Phillip A. Sharp
- Robert Langer
- M. Manoharan
- Eugene V. Koonin
- David P. Bartel
- Margaret S. Ebert
- Isaac Bentwich
- K. Reddy
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
- PCSK9: a convertase that coordinates LDL catabolism Published, JLR Papers in Press, November 19, 2008. (2009, background): “A mutation in PCSK9 (C6793) that prevents folding of the C-terminal domain does not prevent autocatalytic cleavage, suggesting that cleavage is cotranslational (3).”
- In vivo genome editing using Staphylococcus aureus Cas9 (2015, background): “Inhibitors of the human convertase PCSK9 have emerged as a promising new class of cardioprotective drugs after human genetic studies revealed that loss of PCSK9 is associated with a reduced risk of cardiovascular disease and lower levels of LDL cholesterol 39–41 .”
- INCREASED HEPATIC SYNTHESIS AND DYSREGULATION OF CHOLESTEROL METABOLISM IS ASSOCIATED WITH THE SEVERITY OF NONALCOHOLIC FATTY LIVER DISEASE (2012, background): “PCSK9 is a known inhibitor of LDLR expression (Horton et al., 2007).”
- Therapeutic RNAi targeting PCSK9 acutely lowers plasma cholesterol in rodents and LDL cholesterol in nonhuman primates (2008, background): “Mechanistic studies addressing the function of PCSK9 in mice and humans have demonstrated that overexpression or gain-of-function mutations in PCSK9 reduced low density lipoprotein receptor (LDLR) protein levels in liver, which significantly increased circulating plasma cholesterol both in mice and ”
- Approaches to efficiently estimate solvation and explicit water energetics in ligand binding: the use of WaterMap (2013, neutral): “Pearlstein et al. [83] applied WaterMap to detect hydration sites on the binding surface of the LDL receptor (LDL-R) into proprotein convertase subtilisin--kexin type 9 (PCSK9) [84].”