The Harvey rat sarcoma (HRAS) proto-oncogene belongs to the RAS family and is one of the pathogenic genes that cause cancer. Deleterious nsSNPs might have adverse consequences at the protein level. This study aimed to investigate deleterious nsSNPs in the HRAS gene in predicting structural alterations associated with mutants that disrupt normal protein–protein interactions. Functional and structural analysis was employed in analyzing the HRAS nsSNPs. Putative post-translational modification sites and the changes in protein–protein interactions, which included a variety of signal cascades, were also investigated. Five different bioinformatics tools predicted 33 nsSNPs as “pathogenic” or “harmful”. Stability analysis predicted rs1554885139, rs770492627, rs1589792804, rs730880460, rs104894227, rs104894227, and rs121917759 as unstable. Protein–protein interaction analysis revealed that HRAS has a hub connecting three clusters consisting of 11 proteins, and changes in HRAS might cause signal cascades to dissociate. Furthermore, Kaplan–Meier bioinformatics analyses indicated that the HRAS gene deregulation affected the overall survival rate of patients with breast cancer, leading to prognostic significance. Thus, based on these analyses, our study suggests that the reported nsSNPs of HRAS may serve as potential targets for different proteomic studies, diagnoses, and therapeutic interventions focusing on cancer.

Phytochemical investigation on the bark of Nauclea officinalis led to the isolation of a new monoterpenoid indole alkaloid, nauclediol. The structure of the compound was identified through extensive spectroscopic analysis. Nauclediol displayed cholinesterase-inhibitory activities towards AChE and BChE with IC₅₀ values of 15.429 and 8.756 µM, respectively. Statistical analysis revealed that the mode of inhibition of nauclediol was non-competitive inhibitor for both AChE and BChE. Molecular docking revealed that nauclediol interacts with the choline-binding site and the catalytic triad of TcAChE and hBChE. This study also demonstrated the neuroprotective potential of nauclediol against amyloid beta-induced cytotoxicity and LPS-induced neuroinflammation activity in a dose-dependent manner.