NGS Diagnosis of Lp-PLA2 in Cardiovascular Disease & Insilico Analysis of Human Filamin C Domains 14-15 Mutation G1676R
Keywords:
Cardiovascular Disease, Human Lipoprotein-Associated Phospholipase A2, Filamin C domain, Molecular Docking, therapeutic targets, structural variations, NGS, atherosclerosis.Abstract
This study presents a comprehensive exploration of two key components in cardiovascular health: Human Lipoprotein-Associated Phospholipase A2 (Lp-PLA2), represented by the PDB code 5JAD, and filamin C (FLNC) domain 14-15 with mutation gene G1676R represented by the biological sample 7P0E, and By employing an integrated approach that combines structural, genetic, and functional analyses, this study aims to unravel the multifaceted roles of these enzymes in cardiovascular diseases (CVD) and their potential implications for therapeutic interventions. Initially, our investigation focuses on elucidating the structural and functional characteristics of Lp-PLA2, the enzyme represented by 7P0E, and Filamin C domain 14-15 with PDB Code 5JAD. Through rigorous analysis utilizing various bioinformatics tools and techniques, including Molecular Docking, structural validation, Next-generation Sequencing (NGS), Drug discovery, and functional domain analysis, we reveal the complex protein-ligand interactions of Lp-PLA2 and FLNC. Notably, our findings highlight potential therapeutic targets for both enzymes, with molecular docking analyses indicating promising interactions with various ligands, suggesting avenues for targeted interventions in CVD management. Concurrently, computational analyses and bioinformatics methodologies are employed to explore the genetic landscapes of Lp-PLA2and FLNC, and their implications in cardiovascular health. Structural analyses using Command lines and Python-based software provide insights into the three-dimensional architectures of these enzymes, while BLAST assessments elucidate genetic variations. Furthermore, gene ontology and pathway analyses contextualize their roles within cardiovascular pathways, offering a holistic understanding of their contributions to disease pathogenesis. By integrating structural, genetic, and functional analyses of Lp-PLA2and FLNC, this research advances our understanding of their roles in cardiovascular health. The findings not only provide valuable insights into potential therapeutic targets but also offer directions for future research and the development of targeted interventions aimed at combating the burden of cardiovascular diseases.