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Most melanoma tumors harbor oncogenic mutations in the rapidly accelerated fibrosarcoma B-type ( BRAF ) gene, specifically BRAF V600E mutations, which drive continuous, uncontrolled proliferation 4,5
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NFκB residues Arg50, Arg30, Gln29, and Glu225 (forming a loop at binding pocket) showed energy contribution of −6.63, −2.44, −0.95, and −0.71 kJ/mol with DSF in stable complex formation during the equilibration period, however, due to the larger fluctuation of the loop, the DSF did not form stable interactions with NFκB, and the residues Glu25, Glu22, Glu49, and Lys28 (beta-sheet residues at binding pocket) opposed the interaction with positive energies of 0.81 kJ/mol, 0.93 kJ/mol, 2.20 kJ/mol, and 2.54 kJ/mol