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APOB — PCSK9

Text-mined interactions from Literome

Maxwell et al., Proc Natl Acad Sci U S A 2004 : These results were confirmed in vitro by the demonstration that transfection of Pcsk9 in McA-RH7777 cells caused a reduction in LDLR protein and LDL binding
Maxwell et al., Proc Natl Acad Sci U S A 2005 : Overexpression of PCSK9 in mice leads to increased total and low-density lipoprotein (LDL) cholesterol levels because of a decrease in hepatic LDL receptor (LDLR) protein with normal mRNA levels
Sun et al., Hum Mol Genet 2005 (Carcinoma, Hepatocellular...) : Evidence for effect of mutant PCSK9 on apolipoprotein B secretion as the cause of unusually severe dominant hypercholesterolaemia
Soutar et al., Nat Clin Pract Cardiovasc Med 2007 (Genetic Predisposition to Disease...) : Expression of PCSK9 normally downregulates the LDL-receptor pathway by indirectly causing degradation of LDL-receptor protein, and loss-of-function mutations in PCSK9 result in low plasma LDL levels
Cunningham et al., Nature structural & molecular biology 2007 (Hypercholesterolemia) : PCSK9 may diminish LDL receptors by a mechanism that requires direct binding but not necessarily receptor proteolysis
Fisher et al., J Biol Chem 2007 (Genetic Diseases, Inborn...) : Although PCSK9 controls low density lipoprotein (LDL) receptor ( LDLR ) levels post-transcriptionally, several questions concerning its mode of action remain unanswered ... Finally, we show that LDL diminishes PCSK9 binding to LDLR in vitro and partially inhibits the effects of secreted PCSK9 on LDLR degradation in cell culture
Grefhorst et al., J Lipid Res 2008 : Plasma PCSK9 preferentially reduces liver LDL receptors in mice
Frank-Kamenetsky et al., Proc Natl Acad Sci U S A 2008 : Loss of PCSK9 increases LDLR levels in liver and reduces plasma LDL cholesterol (LDLc) , whereas excess PCSK9 activity decreases liver LDLR levels and increases plasma LDLc
Hedrick et al., Curr Opin Investig Drugs 2009 (Hypercholesterolemia) : PCSK9 ( proprotein convertase subtilisin/kexin type 9 ) mediates the post-translational degradation of the LDL receptor (LDLR) and, as a result, modulates serum levels of LDL-cholesterol (LDL-C)
Strøm et al., Clin Chim Acta 2010 (Hyperlipoproteinemia Type II) : Thus, in the presence of high LDL levels, wild-type-PCSK9 , which has twice the binding affinity of R46L-PCSK9 to bind to the LDLR, may not be significantly more potent in degrading the LDLR than R46L-PCSK9
Wu et al., Mol Cell Biochem 2012 : This paper investigated the effects of ox-LDL on PCSK9 , and the molecular mechanisms of PCSK9 siRNA inhibited apoptosis induced by ox-LDL in human umbilical vein endothelial cells ( HUVECs ), to clarify the role of PCSK9 in atherosclerogenesis ... However, ox-LDL induced HUVEC apoptosis and PCSK9 expression, but not LOX-1 expression, were significantly reduced by PCSK9 siRNA
Ai et al., J Clin Invest 2012 (Hyperinsulinism...) : Regulation of hepatic LDL receptors by mTORC1 and PCSK9 in mice
Saavedra et al., J Biol Chem 2012 : PCSK9 enhances the cellular degradation of the LDL receptor (LDLR) , leading to increased plasma LDL cholesterol
Kosenko et al., J Biol Chem 2013 : LDL also inhibited PCSK9 binding to mutant LDLRs defective at binding LDL