Proprotein Convertase Subtilisin/kexin Type 9 (PCSK9) ELISA Kits

Human Proprotein Convertase Subtilisin/kexin Type 9 (PCSK9) Interaktionspartner

1. Study showed that plasma PCSK9 concentrations increase transiently over time in septic and non-septic critically ill patients and demonstrated that PCSK9 negatively regulates LDLR-mediated uptake of bacterial lipoteichoic acid (LTA) and lipopolysaccharide (LPS) by HepG2 hepatocytes through a lipoprotein (LDL)-dependent mechanism, whereas LRP1 and high-density lipoprotein do not contribute to this uptake pathway.

2. In patients with potential familial hypercholesterolemia, positive correlations between concentrations of Lp(a) and PCSK9, as well as of Lp(a)-PCSK9 plasma complex with large subfractions of intermediate and low-density lipoproteins (IDL-1 and LDL-C), were determined by the low molecular weight apo(a) phenotype.

3. rare variants in LDLR and PCSK9 were associated with the onset age of MI by altering LDL-cholesterol levels

4. Acute-phase plasma PCSK9 levels are associated with levels of inflammation and triglycerides, premature coronary heart disease, and gender in acute myocardial infarction patients without reperfusion therapy. However, it does not predict recurrent cardiovascular events at 1 year.

5. Thus, it is evident that sauchinone reduces hepatic steatosis by downregulating the expression of hepatic PCSK9 via SREBP-2.

6. PCSK9 plays a role lipoprotein metabolism and atherosclerotic cardiovascular disease. Review.

7. in patients with acute myocardial infarction, plasma PCSK9 levels measured during the acute phase predict recurrent cardiovascular events within 1 year

8. The results of the current meta-analysis for the first time indicated the relevance of rs562556 of PCSK9 and lower serum cholesterol levels.

9. Associations for BCO2, PCSK9, and TR1B1 Polymorphism and Lifestyle Factors with Ischemic Stroke

10. PCSK9 association with intestinal secretion and plasma overaccumulation of TRL apoB-48 in men with IR

11. PCSK9 may regulate LOX-1 mediated ox-LDL uptake by the THP-1 derived macrophage via TLR4/NF-kappaB/COX-2/ROS pathway

12. Pathogenic mutations in LDLR, APOB, PCSK9 and LDLRAP1 genes were found in 17 of 225 patients with familial hypercholesterolemia leading to premature myocardial infarction.

13. Variants at the PCSK9 gene locus seem to be the major genetic determinants of plasma PCSK9 levels.

14. Elevated serum level of PCSK9 can be observed in systemic lupus erythematosus patients, especially in those with thickening of carotid intima-media.

15. Identification and in vitro characterization of two new PCSK9 Gain of Function variants found in patients with Familial Hypercholesterolemia.

16. Demonstration of an interaction between PCSK9 and ATF-2, which reduces ATF-2/c-Jun dimerization and ATF-2/c-Jun binding to the IFNbeta enhancer. This novel function of PCSK9 should have important implications in optimizing the clinical use of PCSK9 inhibitors.

17. In this study, the appropriate virus-like particle (VLP)-peptide vaccines targeting proprotein convertase subtilisin/kexin type 9 (PCSK9) were screened. The screening criteria of target peptides were as follows: located in catalytic domain of PCSK9, or regulating the binding of PCSK9 and LDL receptors (LDLR)

18. This finding is associated with a profound FH phenotype and the highest known plasma PCSK9 level reported in a human. This finding also has therapeutic relevance, as elevated PCSK9 levels may limit the efficacy of high-dose statin therapy and also PCSK9 inhibition

19. PCSK9-mAbs could significantly reduce circulating Lp(a) levels.

20. We conclude that the PCSK9 R496W (rs374603772) and D374Y (rs137852912) GOF mutations may be significant risk factors in the development of primary dyslipidemia and may have significant impact on lipid parameters in general population.

Mouse (Murine) Proprotein Convertase Subtilisin/kexin Type 9 (PCSK9) Interaktionspartner

1. Glucagon-Gcgr-Epac2-Rap1 pathway regulates plasma LDL-C metabolism by controlling PCSK9 degradation.

2. PCSK9 is up-regulated in the ischaemic hearts and determines development of infarct size, cardiac function, and autophagy.

3. In an inflammatory milieu, elevated levels of PCSK9 potently stimulate the expression of scavenger receptors (principally LOX-1) and ox-LDL uptake in macrophages, and thus contribute to the process of atherogenesis.

4. The absence of PCSK9 in LDb mice results in decreased lipid and apoB levels, fewer atherogenic LDLs, and marked reduction of atherosclerosis.

5. In this study, the appropriate virus-like particle (VLP)-peptide vaccines targeting proprotein convertase subtilisin/kexin type 9 (PCSK9) were screened...PCSK9Qbeta-003 vaccine obviously decreased plasma total cholesterol in both Balb/c mice and LDLR(+/-) mice

6. In the present study, it was investigated whether ticagrelor reduces oxidized lowdensity lipoprotein (oxLDL)induced endothelial cell apoptosis, an initial step for the development of atherosclerosis(AS), and alleviates AS in apolipoproteinEdeficient (ApoE/) mice by inhibiting the expression of proprotein convertase subtilisin/kexin type 9 (PCSK9)

7. We observed long-term postnatal persistence of edited cells in both models, with reduction of plasma PCSK9 and cholesterol levels following in utero Pcsk9 targeting and rescue of the lethal phenotype of hereditary tyrosinemia type 1 following in utero Hpd targeting

8. High PCSK9 expression is associated with atherosclerosis and liver cancer.

9. Given that overexpression of these LOF PCSK9 variants does not cause UPR activation under normal homeostatic conditions, therapeutic strategies aimed at blocking the autocatalytic cleavage of PCSK9 in the ER represent a viable strategy for reducing circulating PCSK9

10. Data suggest that expression of Pcsk9 and Ldlr in liver and pancreas can be regulated by dietary measures; here, dietary supplementation with quercetin-3-glucoside modulates expression of Pcsk9 and Ldlr in prevention of hyperlipidemia and hyperinsulinemia induced by high dietary cholesterol. (Pcsk9 = proprotein convertase subtilisin/kexin type-9; Ldlr = low-density lipoprotein receptor)

11. The data of the present study demonstrated that the PCSK9 shRNAmediated antiapoptotic effect induced by MCAO in hyperlipidemic mice is associated with ApoER2 downregulation, which may be a potential new therapy for stroke treatment in patients with hyperlipidemia.

12. It was concluded that quercetin inhibits oxLDLinduced lipid droplets in RAW264.7 cells by upregulation of ABCAl, ABCG1, LXRalpha and downregulation of PCSK9, p53, p21 and p16.

13. PCSK9 overexpression in the aorta may promote acute aortic dissection.

14. Genetically determined PCSK9 deficiency might be associated with ectopic fat accumulation.

15. The present study aimed to explore the direct toxicity of proprotein convertase subtilisin/kexin type 9 (PCSK9) to atherosclerosis (AS) and its association with apoptotic endothelial cells.

16. present anti-PCSK9 vaccine induced long-lasting anti-PCSK9 antibody production and improved lipoprotein profiles. Thus, anti-PCSK9 vaccine could become a new option for the treatment of dyslipidemia as a long-acting therapy in future

17. PCSK9 may act as an inflammatory mediator in the pathogenesis of atherosclerosis via TLR4/NF-kappaB signaling pathway.

18. PCSK9, by sustaining smooth muscle cell synthetic phenotype, proliferation, and migration, may play a pro-atherogenic role in the arterial wall

19. PCSK9 inhibits lipoprotein(a) clearance through the LDLR.

20. Use Crispr-Cas system to introduce nonsense variants into PCSK9 to lower blood cholesterol levels.

Pig (Porcine) Proprotein Convertase Subtilisin/kexin Type 9 (PCSK9) Interaktionspartner

1. the PCSK9-gain-of-function mutation induces rapid development of atherosclerosis in peripheral vessels of Ossabaw pigs, which is exacerbated by a high-cholesterol diet.