Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
about
A locked nucleic acid antisense oligonucleotide (LNA) silences PCSK9 and enhances LDLR expression in vitro and in vivoAnnexin A2 is a natural extrahepatic inhibitor of the PCSK9-induced LDL receptor degradationThe proprotein convertase (PC) PCSK9 is inactivated by furin and/or PC5/6A: functional consequences of natural mutations and post-translational modificationsHepatic PCSK9 expression is regulated by nutritional status via insulin and sterol regulatory element-binding protein 1cThe proprotein convertase PCSK9 induces the degradation of low density lipoprotein receptor (LDLR) and its closest family members VLDLR and ApoER2Self-association of human PCSK9 correlates with its LDLR-degrading activitySecreted PCSK9 decreases the number of LDL receptors in hepatocytes and in livers of parabiotic miceAnnexin A2 is a C-terminal PCSK9-binding protein that regulates endogenous low density lipoprotein receptor levelsThe PCSK9 decadeTherapeutic RNAi targeting PCSK9 acutely lowers plasma cholesterol in rodents and LDL cholesterol in nonhuman primatesHepatocyte nuclear factor 1alpha plays a critical role in PCSK9 gene transcription and regulation by the natural hypocholesterolemic compound berberineApolipoprotein B Is an innate barrier against invasive Staphylococcus aureus infectionInhibition of PCSK9: a powerful weapon for achieving ideal LDL cholesterol levelsHypercholesterolemia, low density lipoprotein receptor and proprotein convertase subtilisin/kexin-type 9PCSK9 and triglyceride-rich lipoprotein metabolismFrom evolution to revolution: miRNAs as pharmacological targets for modulating cholesterol efflux and reverse cholesterol transportMechanisms and genetic determinants regulating sterol absorption, circulating LDL levels, and sterol elimination: implications for classification and disease riskProfile of evolocumab and its potential in the treatment of hyperlipidemiaProprotein convertase subtilisin/kexin type 9: from the discovery to the development of new therapies for cardiovascular diseasesCholesterol: the good, the bad, and the ugly - therapeutic targets for the treatment of dyslipidemiaMolecular biology of PCSK9: its role in LDL metabolismStructural and biophysical studies of PCSK9 and its mutants linked to familial hypercholesterolemiaThe self-inhibited structure of full-length PCSK9 at 1.9 A reveals structural homology with resistin within the C-terminal domainA proprotein convertase subtilisin/kexin type 9 neutralizing antibody reduces serum cholesterol in mice and nonhuman primatesA PCSK9-binding antibody that structurally mimics the EGF(A) domain of LDL-receptor reduces LDL cholesterol in vivoGenome-wide significant loci: how important are they? Systems genetics to understand heritability of coronary artery disease and other common complex disordersPCSK9 (Proprotein convertase subtilisin/kexin type 9) inhibitors: past, present, and the futureThe proprotein convertases and their implication in sterol and/or lipid metabolismCatalytic activity is not required for secreted PCSK9 to reduce low density lipoprotein receptors in HepG2 cellsIn vivo evidence that furin from hepatocytes inactivates PCSK9Conversion of low density lipoprotein-associated phosphatidylcholine to triacylglycerol by primary hepatocytesPCSK9 regulates neuronal apoptosis by adjusting ApoER2 levels and signalingImplication of the proprotein convertase NARC-1/PCSK9 in the development of the nervous systemEvidence for positive selection in the C-terminal domain of the cholesterol metabolism gene PCSK9 based on phylogenetic analysis in 14 primate speciesMolecular analysis and intestinal expression of SAR1 genes and proteins in Anderson's disease (Chylomicron retention disease)The multifaceted proprotein convertases: their unique, redundant, complementary, and opposite functionsProprotein convertase subtilisin/kexin type 9 (PCSK9) gene is a risk factor of large-vessel atherosclerosis stroke.Histone deacetylase inhibitors: a new mode for inhibition of cholesterol metabolism.Differential proteomics profiling identifies LDPs and biological functions in high-fat diet-induced fatty livers.Fenofibrate treatment increases human serum proprotein convertase subtilisin kexin type 9 levels.
P2860
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P2860
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
description
2005 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
article publié dans les Procee ...... f the United States of America
@fr
artículu científicu espublizáu en 2005
@ast
im April 2005 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 2005/04/12)
@sk
vědecký článek publikovaný v roce 2005
@cs
wetenschappelijk artikel (gepubliceerd op 2005/04/12)
@nl
наукова стаття, опублікована у квітні 2005
@uk
name
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
@ast
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
@en
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
@nl
type
label
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
@ast
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
@en
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
@nl
prefLabel
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
@ast
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
@en
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
@nl
P2093
P2860
P3181
P356
P1476
Decreased plasma cholesterol and hypersensitivity to statins in mice lacking Pcsk9
@en
P2093
David E. Curtis
Jay D. Horton
Norma N. Anderson
Rita Garuti
Robert E. Hammer
Shirya Rashid
Young-Ah Moon
Yuriy Bashmakov
P2860
P304
P3181
P356
10.1073/PNAS.0501652102
P407
P577
2005-04-12T00:00:00Z