GoPubMed Proteins lists recent and important papers and reviews for
proteins. Page last changed on 19 Dec 2016.
Proprotein convertase subtilisin/kexin type 9
PCSK9, proprotein convertase subtilisin/kexin type 9, FH3
This gene encodes a proprotein convertase belonging to the proteinase K subfamily of the secretory subtilase family. The encoded protein is synthesized as a soluble zymogen that undergoes autocatalytic intramolecular processing in the endoplasmic reticulum. The protein may function as a proprotein convertase. This protein plays a role in cholesterol homeostasis and may have a role in the differentiation of cortical neurons. Mutations in this gene have been associated with a third form of autosomal dominant familial hypercholesterolemia (HCHOLA3). [provided by RefSeq, Jul 2008] (from
NCBI)
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Top mentioned proteins:
LDL receptor, apolipoprotein B, CAN, HDL, HAD
Papers using
PCSK9
antibodies
Transgenic expression of cholesterol-7-alpha-hydroxylase prevents atherosclerosis in
C57BL/6J mice
Supplier
In Molecular Therapy. Nucleic Acids, 2001
... PCSK9 western blotting was performed at room temperature for 1 hour with a primary anti-rabbit PCSK9 antibody (1:200; Abcam, Cambridge, UK) ...
cDNA sequence and tissue distribution of the mRNA for bovine and murine p11, the S100-related light chain of the protein-tyrosine kinase substrate p36 (calpactin I).
Supplier
In PLoS ONE, 1986
... Human PCSK9 with a C-terminal V5 tag and wild type (WT) or mutant AnxA2 cDNAs with a HA-tag were subcloned into pIRES2-EGFP vector (Clontech) and used to perform ...
Papers on
PCSK9
Significance of Monoclonal PCSK9-Antibodies - New Approaches to the Therapy of Hypercholesterolemia.
Review
New
Germany. In Blood Purif, Feb 2016
A new therapeutic approach seems to be the modulation of the proprotein convertase subtilisin/kexin type 9 (PCSK9), which reduces the number of LDL-receptors at the cell membrane of the liver cells and thus increases the concentration of LDL-C in the blood.
Synthesis and Characterization of Fatty Acid Conjugates of Niacin and Salicylic Acid.
New
In J Med Chem, Feb 2016
The fatty acid niacin conjugate 5 has been shown to be an inhibitor of the sterol regulatory element binding protein (SREBP), a key regulator of cholesterol metabolism proteins such as PCSK9, HMG-CoA reductase, ATP citrate lyase and NPC1L1.
Genome-wide association study of serum lipids confirms previously reported associations as well as new associations of common SNPs within PCSK7 gene with triglyceride.
New
Tokyo, Japan. In J Hum Genet, Feb 2016
Our present data suggest that PCSK7 as well as PCSK9 may be associated with lipids, especially triglyceride, and may serve as a candidate for a new drug target to treat lipid abnormality syndromes.Journal of Human Genetics advance online publication, 14 January 2016; doi:10.1038/jhg.2015.170.
60 YEARS OF POMC: From the prohormone theory to proopiomelanocortin and to proprotein convertases (PCSK1 to PCSK9).
Review
New
Montréal, Canada. In J Mol Endocrinol, Feb 2016
Thus, what started five decades ago as a theory based on POMC fragments, has opened up novel and productive avenues of biological and medical research, including, for our own current interest, a highly intriguing hypocholesterolemic Gln152His PCSK9 mutation in French Canadian families.
Increased Plasma PCSK9 Levels Are Associated with Reduced Endotoxin Clearance and the Development of Acute Organ Failures during Sepsis.
Review
New
Vancouver, Canada. In J Innate Immun, Feb 2016
PURPOSE: We have recently shown that PCSK9 reduces the clearance of endotoxin and is therefore a critical regulator of the innate immune response during infection.
Safety and efficacy of LY3015014, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9): a randomized, placebo-controlled Phase 2 study.
New
Cleveland, United States. In Eur Heart J, Feb 2016
AIMS: The objective of this study was to evaluate the efficacy, safety, and tolerability of LY3015014 (LY), a neutralizing antibody of proprotein convertase subtilisin/kexin type 9 (PCSK9), administered every 4 or 8 weeks in patients with primary hypercholesterolaemia, when added to a background of standard-of-care lipid-lowering therapy, including statins.
[Cholesterol and atherosclerosis. Historical considerations and treatment].
New
Mexico. In Arch Cardiol Mex, Feb 2016
Despite, the recognition of historical events for 200 years, starting with Michel Chevreul naming «cholesterol»; later on, Lobstein coining the term atherosclerosis and Marchand introducing it, Anichkov identifying cholesterol in atheromatous plaque, and Brown and Goldstein discovering LDL receptor; as well as the emerging of different drugs, such as fibrates, statins and cetrapibs this decade, promising to increase HDL and the most recent ezetimibe and anti-PCSK9 to inhibit the degradation of LDL receptor, however morbidity has not been reduced in cardiovascular disease.
Alirocumab (Praluent): First in the New Class of PCSK9 Inhibitors.
New
In P T, Jan 2016
Alirocumab (Praluent): first in the new class of PCSK9 inhibitors.
PCSK9 inhibitors and cardiovascular disease: heralding a new therapeutic era.
Review
New
New York City, United States. In Curr Opin Lipidol, Dec 2015
PURPOSE OF REVIEW: The first monoclonal antibodies targeting proprotein convertase subtilisin/kexin type 9 (PCSK9) have been approved for clinical use.
Analysis of loss-of-function variants and 20 risk factor phenotypes in 8,554 individuals identifies loci influencing chronic disease.
New
Impact
Houston, United States. In Nat Genet, Jun 2015
To test this hypothesis, we sequenced the exomes of 8,554 individuals and analyzed the effects of predicted LOF variants on 20 chronic disease risk factor phenotypes. Analysis of this sample as discovery and replication strata of equal size verified two relationships in well-studied genes (PCSK9 and APOC3) and identified eight new loci.
Efficacy and safety of alirocumab in reducing lipids and cardiovascular events.
New
Impact
Chilly-Mazarin, France. In N Engl J Med, May 2015
BACKGROUND: Alirocumab, a monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9), has been shown to reduce low-density lipoprotein (LDL) cholesterol levels in patients who are receiving statin therapy.
Efficacy and safety of evolocumab in reducing lipids and cardiovascular events.
New
Impact
Cape Town, South Africa. In N Engl J Med, May 2015
BACKGROUND: Evolocumab, a monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9), significantly reduced low-density lipoprotein (LDL) cholesterol levels in short-term studies.
Inhibition of PCSK9 with evolocumab in homozygous familial hypercholesterolaemia (TESLA Part B): a randomised, double-blind, placebo-controlled trial.
New
Impact
Johannesburg, South Africa. In Lancet, Feb 2015
Evolocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), reduced LDL cholesterol by 16% in a pilot study.
Lipids, blood pressure and kidney update 2015.
Review
Łódź, Poland. In Lipids Health Dis, 2014
However, for the statin-intolerant patients and those patients requiring essential reductions in LDL-C to achieve their goals, new therapies, including PCSK9 inhibitors remain promising drugs.
The LXR-Idol axis differentially regulates plasma LDL levels in primates and mice.
Impact
Los Angeles, United States. In Cell Metab, 2014
The LXR-regulated E3 ubiquitin ligase IDOL controls LDLR receptor stability independent of SREBP and PCSK9, but its relevance to plasma lipid levels is unknown.
Immunization against proprotein convertase subtilisin-like/kexin type 9 lowers plasma LDL-cholesterol levels in mice.
GeneRIF
Roma, Italy. In J Lipid Res, 2012
immunization with human-PCSK9 in mice is able to raise antibodies that cross-react and neutralize circulating mouse-PCSK9 protein thus resulting in increased liver LDL receptor levels and plasma cholesterol uptake
Serum levels of proprotein convertase subtilisin/kexin type 9 in subjects with familial hypercholesterolemia indicate that proprotein convertase subtilisin/kexin type 9 is cleared from plasma by low-density lipoprotein receptor-independent pathways.
GeneRIF
Oslo, Norway. In Transl Res, 2012
In humans, plasma PCSK9 is cleared by LDLR-independent mechanisms.
Peroxisome Proliferator-activated receptor γ activation by ligands and dephosphorylation induces proprotein convertase subtilisin kexin type 9 and low density lipoprotein receptor expression.
GeneRIF
Taiwan. In J Biol Chem, 2012
Results indicate that although PPARgamma activation increased PCSK9 expression, PPARgamma activation induced LDLR and CYP7A1 expression that enhanced LDL cholesterol metabolism.
Proprotein convertase subtilisin/kexin type 9 interacts with apolipoprotein B and prevents its intracellular degradation, irrespective of the low-density lipoprotein receptor.
GeneRIF
Houston, United States. In Arterioscler Thromb Vasc Biol, 2012
propose a new role for PCSK9 that involves shuttling between apoB and low-density lipoprotein receptor
Design and rationale of the LAPLACE-TIMI 57 trial: a phase II, double-blind, placebo-controlled study of the efficacy and tolerability of a monoclonal antibody inhibitor of PCSK9 in subjects with hypercholesterolemia on background statin therapy.
GeneRIF
Boston, United States. In Clin Cardiol, 2011
Describe design of randomized controlled trial using PCSK9 inhibitor for the treatment of hypercholesterolemia.
