convertase


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convertase

 [kon-ver´tās]
an enzyme of the complement system that activates specific components of the system.

con·ver·tase

(kon'ver-tāz),
Proteases of complement that convert one component into another through enzymatic cleavage.
See: component of complement.

convertase

(1) Classical complement pathway C3/C5 convertase, EC 3.4.21.43.
(2) Alternate complement pathway C3/C5 convertase, EC 3.4.21.47.

con·ver·tase

(kon-vĕr'tās)
Proteases of complement that convert one component into another.
See: component of complement
References in periodicals archive ?
Proprotein convertase subtilisin/kexin type 9 (PCSK9) modulates low density lipoprotein cholesterol (LDL-C) concentrations by binding to hepatic LDL receptors, facilitating their catabolism [1], thereby increasing circulating LDL-C.
Statins and ezetimibe modulate plasma proprotein convertase subtilisin kexin-9 (PCSK9) levels.
Effects of Stress Conditions on Subtilisin-like Proprotein Convertase Expression.
Understanding of posttranscriptional LDLr regulation was significantly bolstered by the more recent discovery of proprotein convertase subtilisin/kexin type 9 (PCSK9) protein, a serine endoprotease that promotes degradation of the LDLr protein [13].
When complement proteins are triggered into action by a microbe, the proteins ultimately form a complex enzyme called C3 convertase, which triggers a cascade of immune and inflammatory reactions.
Paired Basic Amino Acid Cleaving Enzyme 4 (PACE4) is a eukaryotic endoprotease in the subtilisin-like proprotein convertase (SPC) family.
According to the partnership, Praluent inhibits the binding of PCSK9 (proprotein convertase subtilisin/kexin type 9) to the LDL receptor and thereby increases the number of available LDL receptors on the surface of liver cells to clear LDL, which lowers LDL-C levels in the blood.
The Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk (FOURIER) trial was the pivotal efficacy and safety study for the proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitor evolocumab (Repatha) and enrolled patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of at least 70 mg/dL (N Engl J Med.
The high cost of PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibition remains a challenge because it is meant for lifelong use, and "the potential increase in health care expenditures at current or even moderately discounted prices could be staggering," wrote Dr.
The genetic causes of FH and related autosomal-dominant hypercholesterolemias include mutations in LDLR (low density lipoprotein receptor), [6] of which >1200 have hitherto been described, and less commonly mutations in APOB (apolipoprotein B) and PCSK9 (proprotein convertase subtilisin/kexin type 9) (1, 2).