Comparative bioinformatics analysis and functional characteristics of natriuretic peptide B (NPPB) gene in humans

The genetic variations affect the prognosis and susceptibility to heart failure and congenital heart disease (CHD). The NPPB gene encodes B-type natriuretic peptide (BNP), which contributes to the upregulation of the ventricular myocardium during cardiac stress, indicating its relevance to heart-related conditions. Despite ongoing structural analysis, NPPB polymorphism affects natriuretic peptide levels, including BNP and NT-proBNP. The heritability of circulating NT-proBNP is influenced by genetic factors. This is the first thorough bioinformatic analysis of the NPPB gene. The molecular formula of the NPPB protein is C638H1051N199O189S60, which is shown by its physicochemical properties to be hydrophilic, negatively charged, and highly unstable. The gene mania study built gene-to-gene interaction networks including NPPB by finding 8 interacting genes and offering insights into the broader regulatory processes. HuRI and STRING analysis also served to perform a PPI network analysis, which showed links to other proteins that help explain underlying diseases and intricate physiological processes. The α-helix is predicted by the secondary structure comprising 41.04% of the core structure; however, Phyre2 discovered that the α-helix makes up 28% of the core structure and that 72% of the sequence is anomalous. Furthermore, the prevalence of α-helices relative to β-type structures highlights significant structural characteristics associated with the functional NPPB elements. The 3D structure was generated for homology modelling using the SwissModel server, and the model quality was confirmed using QMEAN, ProSA, and SAVES analysis. The LigPlot+ tool and Discovery Studio were used to examine possible interactions between the ligands and the NPPB protein. Targeting the NPPB protein, the discovered ligands (pigenin, GN8, Rofecoxib, Sclareol, and Visotriazine) with favourable binding energies show promise for potential treatments. From our findings, a broad spectrum of molecules may be investigated in targeted docking studies as potential treatments for NPPB-driven disease. Determining the functional value of NPPB and designing future experimental research to validate these expected interactions and look into their biological consequences requires knowledge of such molecular interactions.