Dwight V. Nissley

This study analyzes the free energy and flexibility of autoinhibited human BRAF using molecular dynamics simulations based on a cryo-EM model to understand its activation mechanism.

This study develops an in vitro BRAF activation assay to elucidate molecular mechanisms of BRAF disassembly and identifies RAS binding as critical for activation.

This study uses deep mutational scanning to analyze KRAS variants, identifying gain- and loss-of-function mechanisms and their impact on oncogenic activity.

The paper identifies a novel NRAS internal tandem duplication in colorectal cancer that disrupts GAP-binding, leading to sustained RAS activation and oncogenic signaling.