anti-Proprotein Convertase Subtilisin/kexin Type 9 (PCSK9) Antibodies

Human Proprotein Convertase Subtilisin/kexin Type 9 (PCSK9) interaction partners

1. Circulating PCSK9 concentration as a continuous variable was not significantly associated with the risk of cardiovascular events. More well-designed studies are needed to clarify the role of PCSK9 in cardiovascular risk.

2. Data indicate that the elevation in plasma apoB-48 (show APOB Antibodies) levels associated with FH is independent of PCSK9 levels.

3. we discuss current experimental and clinical evidence of the role of PCSK9 and its inhibition on lipid metabolism and several pathologic conditions with a focus on clinical outcomes--{REVIEW}

4. The E670G polymorphism of the PCSK9 gene is associated with the lipid levels and risk for coronary heart disease.

5. Here, we assess the available evidence for the association of PCSK9 status with the incidence and control of diabetes mellitus in preclinical and clinical studies, and identify molecular mechanisms regulating PCSK9 expression in the diabetic state. [Review]

6. These results demonstrated the molecular mechanisms of how HCV modulates PCSK9 promoter activity and advanced our understanding on the mutual interactions between HCV and PCSK9.

7. These findings provide useful information for researchers interested in the fields of PCSK9 genetics and cardiovascular risk prediction not only for designing future studies, but also for clinical and public health applications

8. Circulating PCSK9 is significantly related to arterial stiffness, independent of sex and menopausal status in women.

9. Study demonstrated PCSK9 as a direct target of miR (show MLXIP Antibodies)-224 and increased miR (show MLXIP Antibodies)-224 or decreased PCSK9 could promote apoptosis and suppress proliferation, invasion of tumor cell line in pancreatic neuroendocrine neoplasms.

10. There are no associations between PCSK9 levels and either glucose or lipid homeostasis parameters. Nevertheless, a statistically significant link was observed between PCSK9 and markers of insulin (show INS Antibodies) homeostasis, solely in CF patients who presented normal glucose tolerance.

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

1. 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

2. PCSK9 may act as an inflammatory mediator in the pathogenesis of atherosclerosis via TLR4 (show TLR4 Antibodies)/NF-kappaB (show NFKB1 Antibodies) signaling pathway.

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

4. PCSK9 inhibits lipoprotein(a) clearance through the LDLR (show LDLR Antibodies).

5. Use Crispr-Cas (show CTNND1 Antibodies) system to introduce nonsense variants into PCSK9 to lower blood cholesterol levels.

6. Studied the combination model of a single AAV-PCSK9 injection, high-fat diet, and partial carotid ligation which induces robust atherosclerosis in the flow-disturbed carotid artery within 3 weeks in C57 mice, and results suggest this is a quick and convenient model to study atherosclerosis and mechanisms using any knockout or transgenic mice without having to generate double knockouts.

7. These observations suggest positive feedback interplay between SMC (show DYM Antibodies)-derived PCSK9 and mtDNA damage in the proinflammatory milieu involving mtROS. This interaction results in cellular injury, characterized by apoptosis-a hallmark of atherosclerosis.

8. AdipoR activation by agonists regulated PCSK9 expression and inhibits atherosclerosis in apoE (show APOE Antibodies)(-/-) mice.

9. Adeno (show ADORA2A Antibodies)-associated virus mediated infection with a mouse PCSK9 gain-of-function mutation is a rapid, easy, and efficient approach for inducing hypercholesterolemia and promoting abdominal aortic aneurysms in C57BL/6 mice infused with angiotensin II.

10. conditions that cause ER stress regardless of their ability to dysregulate ER Ca(2 (show CA2 Antibodies)+) inhibit PCSK9 secretion, thereby reducing PCSK9-mediated LDLR (show LDLR Antibodies) degradation and promoting LDLR (show LDLR Antibodies)-dependent hepatic cholesterol uptake.