gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Apolipoprotein C-II

apolipoprotein C-II
cofactor and activator of lipoprotein lipase; crucial for the hydrolysis of triacylglycerols and very-low-density lipoproteins; mRNA found mainly in the liver [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Lipoprotein Lipase, HAD, ACID, Apo, CAN
Papers on apolipoprotein C-II
Apolipoprotein C-II Adopts Distinct Structures in Complex with Micellar and Submicellar Forms of the Amyloid-Inhibiting Lipid-Mimetic Dodecylphosphocholine.
Curtain et al., Australia. In Biophys J, Feb 2016
Thus, we have used the apolipoprotein C-II amyloid model system in conjunction with x-ray and neutron scattering analyses to address this problem.
Targeted Proteomics Identifies PON1 and Apolipoprotein Cs as Potential Risk Factors for Hypoalphalipoproteinemia in Diabetic Subjects Treated with Fenofibrate and Rosiglitazone.
Heinecke et al., Washington, D.C., United States. In Mol Cell Proteomics, Jan 2016
This approach demonstrated marked increases in the relative concentrations of paraoxonase/arylesterase 1 (PON1), apolipoprotein C-II (APOC2), apolipoprotein C-I, and apolipoprotein H in the HDL of subjects who developed hypoalphalipoproteinemia.
Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis.
Morita, Japan. In Biol Pharm Bull, Dec 2015
Chylomicron remnants and VLDL remnants are produced by the lipoprotein lipase-mediated lipolysis of triglycerides, which is activated by apolipoprotein C-II bound on the particle surfaces.
Hydrogen/Deuterium Exchange and Molecular Dynamics Analysis of Amyloid Fibrils Formed by a D69K Charge-Pair Mutant of Human Apolipoprotein C-II.
Gooley et al., Melbourne, Australia. In Biochemistry, Sep 2015
To reconcile the dual abilities of apolipoproteins to form either α helices or cross-β sheet structures, we examined fibrils formed by human apolipoprotein C-II (apoC-II).
Development of multiplex mass spectrometric immunoassay for detection and quantification of apolipoproteins C-I, C-II, C-III and their proteoforms.
Nedelkov et al., Tempe, United States. In Methods, Jul 2015
Described here is the development of a multiplex mass spectrometric immunoassay (MSIA) for quantification of apolipoprotein C-I (apoC-I), apolipoprotein C-II (apoC-II), apolipoprotein C-III (apoC-III) and their proteoforms.
Chylomicronaemia--current diagnosis and future therapies.
Hegele et al., London, Canada. In Nat Rev Endocrinol, Jun 2015
The first form is very rare monogenic early-onset chylomicronaemia, which presents in childhood or adolescence and is often caused by homozygous mutations in the gene encoding lipoprotein lipase (LPL), its cofactors apolipoprotein C-II or apolipoprotein A-V, the LPL chaperone lipase maturation factor 1 or glycosylphosphatidylinositol-anchored high density lipoprotein-binding protein 1.
Association of lecithin-cholesterol acyltransferase activity measured as a serum cholesterol esterification rate and low-density lipoprotein heterogeneity with cardiovascular risk: a cross-sectional study.
Hirayama et al., Tokyo, Japan. In Heart Vessels, May 2015
Multivariate regression analysis after adjustments for traditional risk factors identified elevated TRL-related marker (TG, remnant-like particle cholesterol, apolipoprotein C-II, and apolipoprotein C-III) levels as independent predictors of smaller-sized LDL particle size, both in the overall subject population and in the subset of patients with serum LDL cholesterol levels of <100 mg/dL.
A 3-day-old neonate with severe hypertriglyceridemia from novel mutations of the GPIHBP1 gene.
Calandra et al., Roma, Italy. In J Clin Lipidol, Mar 2015
Intravascular lipolysis involves the TG-hydrolase lipoprotein lipase (LPL) as well as other factors such as apolipoprotein CII and apolipoprotein AV (activators of LPL), GPIHBP1 (the molecular platform required for LPL activity on endothelial surface), and LMF1 (a factor required for intracellular formation of active LPL).
Plasma clusterin as a candidate pre-diagnosis marker of colorectal cancer risk in the Florence cohort of the European Prospective Investigation into Cancer and Nutrition: a pilot study.
Palli et al., Milano, Italy. In Bmc Cancer, 2014
Eight proteins including apolipoprotein C-II, complement C4-B, complement component C9, clusterin, alpha-2-HS-glycoprotein, mannan-binding lectin serine-protease, mannose-binding protein C, and N-acetylmuramoyl-L-alanine amidase were selected as promising candidate biomarkers.
Screening High Abundance of Peptide for Making Examination Possible in Human Urine.
Zhang et al., Beijing, China. In Ann Clin Lab Sci, 2014
There were 15 peptides passed though the threshold and they were identified as fragments of fibrinogen alpha chain precursor, vitronectin precursor, inter-alpha-trypsin inhibitor heavy chain H4, complement component 3, prothrombin, apolipoprotein C-II, and alpha-fetoprotein.
[Primary hyperchylomicronemia].
Yamashita, Ōsaka, Japan. In Nihon Rinsho, 2013
This entity includes familial lipoprotein lipase (LPL) deficiency, familial apolipoprotein C-II deficiency, primary type V hyperlipoproteinemia, and idiopathic hyperchylomicronemia. Idiopathic hyperchylomicronemia is caused by an LPL inhibitor or autoantibody against LPL.
A review of the role of apolipoprotein C-II in lipoprotein metabolism and cardiovascular disease.
Elisaf et al., Ioánnina, Greece. In Metabolism, 2012
The focus of this review is on the role of apolipoprotein C-II (apoC-II) in lipoprotein metabolism and the potential effects on the risk of cardiovascular disease (CVD).
[Therapeutic application of diacylglycerol oil for the metabolic syndrome].
Tada et al., Ichikawa, Japan. In Rinsho Byori, 2010
Further, our another study using the apolipoprotein C-II deficient subject demonstrated that DAG suppressed postprandial increase in VLDL-cholesterol and remnant-like particle-cholesterol compared with TAG, suggesting that DAG suppress postprandial TG-rich lipoprotein independent of lipoprotein lipase.
Inheritance of apolipoprotein C-II deficiency with hypertriglyceridemia and pancreatitis.
Little et al., In N Engl J Med, 1979
A study of the relatives of a patient with apolipoprotein C-II deficiency showed that the defect is inherited as an autosomal recessive trait.
Hypertriglyceridemia associated with deficiency of apolipoprotein C-II.
Poapst et al., In N Engl J Med, 1978
An apolipoprotein activator (apolipoprotein C-II) for lipoprotein lipase could not be detected by polyacrylamide-gel electrophoresis of apoproteins, immunodiffusion of the plasma against anti-apolipoprotein CII or activation assays for lipoprotein lipase.
share on facebooktweetadd +1mail to friends