@article {2208,
	title = {Unveiling Potential Therapies: Molecular Docking Analysis of CAMKK2 and Its Mutant Variants with CAMKK2 Inhibitors in Indonesian Patients with HIV-Sensory Neuropathy},
	journal = {Pharmacognosy Journal},
	volume = {16},
	year = {2024},
	month = {February 2024},
	pages = {46-51},
	type = {Original Article},
	chapter = {46},
	abstract = {<p class="rtejustify">HIV sensory neuropathy (HIV-SN) is one among many complications that impair patients{\textquoteright} quality of life. Studies in Asian and African populations found that single nucleotide polymorphisms (SNPs) of calcium/ calmodulin-dependent protein kinase 2 (CAMKK2) influence the risk of HIV-SN. This study attempts to explain the influence of CAMKK2 mutations on HIV SN by studying bioinformatics interactions between CAMKK2, its mutants, and their inhibitors by molecular docking with AutoDock in order to observe their interactions with CAMKK2 inhibitors. Results showed that CAMKK2{\textquoteright}s binding energy with its native ligand (ATP) is stronger than the mutant variant of CAMKK2MT85 and CAMKK2MT363. Conversely, interaction between CAMKK2 and its inhibitors (KN-93, STO-609, and trifluoperazine) have the lowest mean binding energy compared to CAMKK2MT85 and CAMKK2MT363. This indicates that the mutant variants have weaker interactions with the native ligand and the inhibitors, therefore disrupting the normal function of CAMKK2, its interactions with the inhibitors, while increasing the likelihood of HIV-SN.</p>
},
	keywords = {CAMKK2 inhibitors, HIV-SN, Molecular docking, mutation, SNP},
	doi = {10.5530/pj.2024.16.7},
	author = {Ahmad Yanuar Safri and Salim Harris and Putera Dewa Haryono and Ariane Benina Budiwan and Eugenia Isadora and Aisyah Fitriannisa Prawiningrum and Fadilah Fadilah}
}
