Exploring LDLR-APOB Interactions in Familial Hypercholesterolemia in the Vietnamese Population: A Protein-Protein Docking Approach.

ABSTRACT: Atherosclerotic cardiovascular diseases (CVDs) are closely linked to factors such as familial hypercholesterolemia (FH), often caused by mutations in low-density lipoprotein receptor (LDLR) and apolipoprotein B (APOB). Through a comprehensive bioinformatic analysis, we identified novel LDLR and APOB mutations and their cardiovascular disease (CVD) implications, focusing on unique variants in the Vietnamese population. We used homology modeling to predict protein structures; in addition, through protein-protein molecular docking, we assessed how these mutations affect binding affinities. We identified 10 novel binding residues exclusive to the wild-type and precursor LDLR isoforms, including ASP-47, GLY-48, and GLU-51. Analyses of 154 complexes revealed 5 isoform

SUBMITTER: Kim NT 

PROVIDER: S-EPMC11605763 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature