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Thus, mutations in the CETP gene associated with CETP deficiency are characterized by high serum HDL-C levels and reduced cardiovascular risk [ 23].
They show a genetic interaction between CETP genotype and LPA; LPA heterozygotes with the CETP IV/II genotypes monotonically decrease in frequency with age, but those in CETP VV individuals increase from age 70 onward.
For example, common variants in the CETP gene, which encodes cholesteryl ester transfer protein, the target of the CETP inhibitor torcetrapib, were associated with the same lipid and lipoprotein changes seen with torcetrapib treatment but were not associated with high blood pressure, an off-target effect of torcetrapib.
In contrast to mice and rats, CETP is expressed in hamster liver which explains raise of serum HDL levels in response to the CETP inhibitor Anacetrabip [ 4].
The molecular docking of HL16 into the CETP was performed.
The peptide exhibits self-binding capability towards the CETP.
Early experiments on mice showed that removing the CETP gene seemed to keep them from developing clogged arteries.
Also, cholesterol may competitively inhibit cholesteryl ester binding to the CETP molecule, with triglyceride binding being largely undisturbed.
The binding mode demonstrated that HL16 occupied the CETP binding site and formed interactions with the key amino acid residues.
A drug that mimics the function of the CETP gene is already in development, says Atzmon, and the same could happen with APCO3.
The structure of human plasma cholesteryl ester transfer protein (CETP) was mapped in silico by a search of the structural effects of missense mutations in the CETP gene.
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